By Slugsie, on May 29th, 2009It’s quite common whilst reading creationist material for them to state that they have no problem with the idea of Microevolution. They’re quite happy with the idea that any given species will have small variations over time – i.e. Darwin’s Finches. But creationists have a major problem with accepting that Micro evolution, plus lots (and lots) of time leads to Macroevolution. They state that it’s impossible for one species to evolve into another species, no matter how many small variations you come up with.
First of, I’d just like to say that to evolutionary biologists there is no difference between the two. Evolution is evolution, the amount of it is irrelevant, it’s the fact of it that counts.
Secondly, I’m not about to come up with some magical evolutionary trick that shows that micro changes will lead to macro changes in an animal. I’m not a biologist, I wouldn’t really know where to begin. But what I can do is show how many small changes can easily make a big difference, even though each change is almost irrelevant.
Imagine you’re utterly destitute, you have not a penny to your name. You are without doubt poor. Now, one day along comes a stranger and gives you a dollar. Now, by any western standards, you’re still undoubtedly poor. Next day, the stranger comes by again, and gives you another dollar. You now have $2, you’re definitely better off than you were two days ago, but poor is still what you are. This stranger keeps coming by, day after day, dollar after dollar. After nearly 3 years, he’s given you around $1000! If we stretch this out a bit, and ignore normal human life-spans after nearly 2800 years you have $1,000,000! By most peoples standards you could be considered a rich man. But when did that happen exactly? If you’re rich at $1,000,000, aren’t you to all intents and purposes rich at $999,999?
The point I’m trying to get across is that each change made little difference to your wealth. Each day you weren’t really any better off than you were the day before. It’s only in the context of thousands of years that you could considered to have become wealthy.
May 29th, 2009 | 
Tags: 
Category: 
The essential difference between micro- and macro- evolution is visible on a closer inspection of the meaning of micro-evolution. In micro-evolution, a species becomes more narrowly defined: through genetic mutation or by losing access to a genetic trait through inbreeding a population loses genetic information. Macro-evolution requires that a population gain genetic information, which does not occur as a part of micro-evolution, regardless of how much micro-evolution occurs.
Joshua, evolution does not make a distinction between micro- and macro-. They’re one and the same. It’s only creationists who try to assert a difference. When a genetic mutation occurs it doesn’t increase or decrease the amount of information, it only alters the expression of that information. Once enough mutations have occurred it makes viable interbreeding between differing population groups impossible – either physically (think Chihuahua and Great Dane) or biologically (think horses and donkeys). Once the interbreeding line is drawn that’s where the species line begins to appear.
There are plenty of very well documented lines of genetic heritage that show many small changes leading to very different species of creature.
I am a trained geneticist and biochemist and I observe a paradox in the theory of evolution that fits this micro/macro-evolution discussion. The paradox is that in cases like that of the Chihuahua and Great Dane it is easy to see and demonstrate that the the chihuahua has less genetic information in its genome than that of the “mutt” from which it evolved. Same with the Great Dane. These dogs were produced from selective breeding which REMOVES certain genes from the newly formed lines. Natural selection produced the same effect on the Galapagos finches, namely, that each distinct line of finches has LESS genetic information than the “mutt” line of finches from which they evolved.
This is the fundamental paradox of the theory of evolution: How can you get new species formed from new genes when the evolutionary mechanism (ie, impediments to gene flow) merely produces sub-species lines which have (1)LESS genes than the parent line and (2) the genes they do have are entirely a sub-set of the genes present in the parent line?
The conclusion that should be drawn from the data that we can see about gene flow, mutations, and evolution is that the original species had the most genetic variation and that as time moves forward we are LOSING genetic information. In essence, we are not evolving toward higher genetic complexity in the biota… rather, it appears that we are de-evolving toward lower complexity.
Tom, intriguing points you make there. As I point out regularly, I’m not a a scientist, so I can’t comment directly on what you say. Is there any chance you could point me in the direction of a paper or article that deals with this so I can try and better educate myself? Thanks.
@Tom, incorrect. The domestic dog has several gene sequences that are not present in the wolf, common ancestor of all dogs, and vice versa. The wolf also has sequences not present in the dog due to the fact that dogs evolved from a sub population of the wolf species.
While it does sometimes happen, we are not simply losing genetic information as we evolve. We are also gaining it, which is why the number of genes for a given organism may not be what you expect given its apparent complexity. Humans and rats have a comparable number of genes, for example, 33,000 and 27,000 respectively (thereabouts). And its what those genes are coded to do and how the interact with each other that builds the complexity that is otherwise unapparent in their numbers alone.
And Slugsie is right. Evolution is evolution. Believing in “micro” evolution but not “macro” is like saying you believe in seconds but not centuries. There is no biological constraint that would prevent small incremental changes from adding up to big changes. If there were, we’d have hit it in the labs by now.
Interesting point, Autumn. Question. What is the latest account scientists want to use to explain where life began?
Are they still going on about the big bang, geodes (yes this one is a real theory), or is it something new now? I mean after all if the scientist can’t keep their details straight how can I, someone who isn’t trained in the sciences.
Doug, the theory of how life began has nothing to do with evolution. Evolution works on the basis that life is already there and is the explanation of how you can go from a single simple lifeform to the huge variety that we currently see all around us.
Evolution has nothing to do with the Big Bang, or any other branch of cosmology. Whilst it is true that the various space sciences do use the term evolution to describe how a dust cloud forms a star and planetary system for example, it’s using the word in to describe change over time, not the biological definition of evolution. It seems to be a common mistake to confuse the two, and just muddies the waters when it comes to trying to educate ‘the masses’ with regards to biological evolution.
You also seem to think that scientific knowledge changing is a bad thing. It isn’t. Science looks at the facts in evidence, and poses a hypothesis that fits the facts. After a while if the hypothesis continues to work it becomes a theory. If a new fact comes along that disproves the theory then either the theory is modified to accomodate the new fact, or the theory is abandoned. It’s one of the beauties of science, the fact that it is self modifying, and self correcting.
Currently scientists don’t really know how life began, and they aren’t afraid to admit it. There are several hypothesis, the strongest one is currently abiogenesis. There have also been a number of ground breaking experiments recently that have demonstrated how organic molecules could spontaneously generate is conditions resembling those thought to exist around the time life arose on Earth.
@Autumn, A more accurate statement about dogs and wolves relative to the theory of evolution is that modern dogs and modern wolves both evolved from some common ancestor. My approach still works in this case. The common ancestor has more genetic information than either the modern wolf or the modern dog. The modern wolf genome would be a subset of the common ancestor. The modern dog genome would be a subset of the common ancestor. There would be lots of overlap between the modern wolf and the modern dog because they came from a common ancestor. This model fits the data. Also, this model (we are losing alleles over time) does not involve a violation of the 2nd law of thermodynamics like the prevailing models do (we are gaining alleles over time). Therefore I contend for it as a theory that better fits the data.
I have a degree in cell/molecular biology and I have seen the books that say \"new alleles CAN form by random mutations\", but none of them show examples of it actually happening. We do, in fact, have a good platform to witness new allele formation if it happens. Inbred mice strains used for lab testing have been inbred to eliminate genetic variation and frequently have their DNA \"read\" as part of the experiments run on them. They have a \"generation\" of about 3 months, meaning that you have about 4 generations per year. The DBA Inbred Strain is the oldest and goes back to 1909. That\’s about 400 generations of the DBA line yet no net new alleles have been reported (some discoveries of existing alleles have been reported in a sub-line called DBA/2 as \"new\" but they were not claimed to a new allele derived from evolutionary processes, rather, they are reporting a previously undiscovered allele at an already known locus). That is despite the fact that the DBA strain shows a high spontaneous mutation rate (I guess they have bad DNA repair proteins).
Which brings me to DNA repair. Spontaneous DNA damage rates are very high (reported at around 1 million lesions per cell per day in humans*). The effect of that damage is not usually noticed because there is an army of proteins whose mission it is to repair DNA. Which came first, the DNA sequence or the proteins that code from DNA to repair the DNA? It\’s an absurd question because the answer has to be DNA. Therefore, if evolution is true, no cell based on DNA could survive for any meaningful time because the DNA would become damaged so fast as to become non-coding and lead to cell death.
As for the beginning of life, it is a mystery to science. But evolution claims to be able to go from single-celled organisms all the way to humans. But the issue of \"which came first\" regarding DNA repair prevents evolution as a process from moving beyond the most rudimentary, RNA-based proto-cells.
* from Lodish H, Berk A, Matsudaira P, Kaiser CA, Krieger M, Scott MP, Zipursky SL, Darnell J. (2004). Molecular Biology of the Cell, p963. WH Freeman: New York, NY. 5th ed
Tom, obviously I can’t comment on most of what you say because you’re so much more versed in it than I am. However I do have to comment on one little thing. The Theory of Evolution and the Second Law of Thermodynamics are in no way in conflict.
@Doug. Doesn’t matter. A 15th century epileptic may not have known, for example, what her condition was, but that doesn’t mean the correct answer was demon possession. We don’t know for a certainty how life began and likewise that doesn’t mean the best answer is creation. Sometimes the best answer is “I don’t know” and a little patience while scientists figure it out. Just because we can ask the question now doesn’t mean we have the answer now. I for one am cool with that.
@Tom, 3rd and 4th paragraphs of your post: Actually, there’s a really easy way around that one. One of the best defenses against UVB radiation is water, and the more of it between you and the radiation, the less radiation you and your DNA are exposed to. This may go a long way to explaining why life is believed to have started in the ocean.
Slugsie, I have certainly seen plenty of bad applications of the 2nd law of thermodynamics as it applies to evolution and I don\’t think that the 2nd law is violated once evolution is able to convert the suns energy into work in a cell (in the form of chemical bonds in sugars). However, my issue with evolution and the 2nd law comes into play prior to the evolution of photosynthesis. Here is my rationale:
At the core, the 2nd law is not about disorder, it is about concentrations of energy. As it relates to biochemistry, organic covalent chemical bonds are concentrations of energy. As such, these chemical bonds are fundamentally unstable because they concentrate energy into a location in which the background energy is lower than the energy resident in the chemical bond. Similar to heat wanting to flow from hot areas to cold areas, the energy concentrated in chemical bonds wants to dissipate. What keeps all these bonds from flying apart? Activation energy – which is the initial energy required to allow the chemical bonds to dissipate its energy concentration. This can be seen when you put a match to a piece of wood. The heat from the match in the presence of oxygen causes the cellulose (principal component of wood) to react with the oxygen. This reaction gives off heat and moves the elements in cellulose and oxygen into a lower energy state (carbon dioxide and water) where the energy trapped in those chemical bonds is much lower, thus the energy has been dissipated in perfect harmony with the 2nd law.
Now lets move to DNA and more specifically, we are interested in the chemical bonds that hold DNA together. These bonds are high energy and susceptible to significant damage from outside energy sources. A common example of damage from outside sources is when UV light hits DNA and forms what is called a thimine dimer. Normally, there is a single phosphodiester bond between bases as you move along the length of a DNA strand. When a thimine dimer occurs a second bond forms between 2 adjacent thimine molecules. This causes the DNA strand to bend sharply and prevents transcription for that location because the 3-dimentional fit necessary for enzyme attachment is no longer as is needed… the enzymes fall off the DNA strand at this point. What does this have to do with the 2nd law? Because we have a vast energy sink in the form of sugars produced from photosynthesis, we have the necessary energy to do exactly what the cell does to fix the thimine dimer. Namely, by expending lots of energy, a dance of enzymes cuts the T-T side of the double helix and rebuilds it from A-A side of the other member strand of the double helix. That\’s not a violation of the 2nd law because the sun\’s energy was converted to sugars, which got transported to a cell (by eating), which were metabolized by the mitochondria to produce ATP and GTP which became the energy sources used to fix the DNA damage. But this all hinges on photosynthesis: no photosynthesis, then no energy to repair DNA.
The 2nd law explicitly applies to closed systems. But it applies equally well to open systems where there is no mechanism to convert the incoming energy into useful work (called transformation as it applies to the 2nd law in open systems). The energy will still dissipate in an open system if you don\’t have transformation going on. Now we are ready to talk about the linkage between the 2nd law and evolution.
A necessary facet of evolution is that cells and DNA existed prior to the evolution of photosynthesis. However, prior to photosynthesis, there was no mechanism to transform the energy from the sun into useful work. Thus, prior to the evolution of photosynthesis, evolution violates the 2nd law. Furthermore, the sun beating down on the surface of the earth would have damaged any DNA that was exposed and without photosynthesis, there would have been no energy source for which to fix the broken DNA.
In a previous comment I talked about DNA not being able to survive early stage evolution without the arsenal of DNA repair proteins. Now we can see that not only do we have to have the repair proteins, but we have to have photosynthesis to be able to supply the energy to have the DNA repair proteins do their job. The next facet is that you have to be able to metabolize the sugars produced by photosynthesis, and to do that you need to evolve metabolic proteins and organelles to extract energy out of the sugars. The simultaneous and spontaneous evolution (encoded into DNA) of all these functions that I am talking about is why evolution cannot bootstrap itself. It requires too much simultaneous coincident. The list I have given is only part of the necessary functions that have to be in place for evolution to go from single-cell to multi-cell organisms. Add to these the simultaneous evolutionary need of transcription, translation, cytoskeleton, cytoskeletal motor, and cell division proteins. The conventional evolutionary model can\’t get beyond single-celled without these.
When a cell looks like a blob of clay (as it did to Darwin), then lots of things seem possible regarding evolution. But when you know what specific role each part of the cell plays and how it\’s all built on DNA, then you start to see how many things had to be in place for the first cell to get off the ground. When you look at it that way, then the cell looks designed.
@Tom, paragraph 2 of your post: OK, so I googled DBA Inbred strain and got this tidbit:
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6W7J-4R2GX3H-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=616f6806767709a13355180200213653
See the abstract below from Elsevier. Wish I could bold some of those sentences:
[quote]The year 2009 is the 100th anniversary of the founding of the first inbred strain of mouse, called DBA. During the last 100 years, inbred strains have proved their value for biomedical research and the number of such strains has mushroomed to over 450, each with different genotypic and phenotypic characteristics and useful for the study of disease and normal function. However, although inbred strains are stable, they are not fixed entities and researchers need to be aware of the phenomena of new mutations and of genetic drift, which occur within all mouse colonies. If the mutations are what we term in this review ‘quiet mutations’, then they might result in rather unexpected and sometimes tremendously valuable results. Here, we discuss these phenomena and look at how new genomic technologies might help us to detect ‘quiet mutations’ and use them to our advantage.[/quote]
These genetic lines are NOT static. The mutations you refer are happening BETWEEN generations, not within an existing organism so they have nothing to do with DNA repair. They are evolution at work and the process by which new alleles are created.
The idea is that two parents with allele 1 can produce offspring with allele 2 or allele 3, even if its extremely rare, and even if it doesn’t do the offspring much good, and EVEN IF that new allele has already been seen in an unrelated organism. It is a mutation and a novel allele as long as it wasn’t inherited from the parents.
Autumn, water can protect DNA from UV, but there are lots of sources of DNA damage. Many are even products of cellular metabolism. Modern cells have organelles and structures to deal with these chemicals, but how would the primordial cells deal with them (like lysosomes, and high acidity associated with respiration)?
Beside that, water is not exactly a happy place for early stage evolution. Every cell metabolizes. This metabolic activity changes its internal pH and salinity. Thus every modern cell has various salt and proton pumps to deal with matching the cells pH and salinity to the outside world. As this relates to water development of early stage evolution, it means that you have to have cellular machinery and structure to deal with pH and salt or the cell dies.
Let\’s play this out.
Let\’s say that an early cell has just enough DNA coding to deal with everything except for cell wall and saline/proton pumps. Every modern bacteria has a cell wall or matrix around it to keep the cell from exploding due to osmosis. Here is why. As the salt levels increase with metabolism, the osmotic pressure inside the cell increases. The cell takes on water until the cell membrane ruptures. If the cell has a fibrous wall or matrix around the outside, then the cell essentially has a fence rapped around it that gives it extra support and allows the cell to have slightly higher saline levels inside the cell versus outside.
Wouldn\’t a developing cell in water have to have a cell wall or matrix to keep from exploding due to internal metabolism changing the pH and saline levels? Well, no, IF the cell can actively keep the right osmotic balance with its environment. But to actively match it\’s environments saline/pH level it would have to have cell receptors for saline/pH, metabolic feedback loops to instruct the cell to actively start pumping ions into or out of the cell to match the external pH/saline.
Furthermore, two trends are demonstrable within the oceans. 1 – the oceans are becoming more salty as rain carries more salt to the ocean and 2 – the oceans appear to be getting more acidic (currently around pH of 8). Therefore, the primordial ocean was likely relatively fresh and relatively alkaline. That\’s a pretty hostile environment for a developing cell with no cell wall or matrix and no ion pumps.
Lastly, the modern theory of how information got coded into DNA has us starting with RNA. But RNA is even less stable in water than DNA. If the RNA isn\’t in a perfect salt and pH solution, the water hydrolyzes the RNA… it cut\’s it into pieces.
Autumn, about inbred mice.
My point is not that mutations don\’t occur. They do. My point is that mutations do not produce net new genetic entities, rather they simply act on existing ones. They don\’t produce new entron, codon and exon sequences. Where are the new coding sequences? New coding sequences MUST occur in order to accumulate genetic information as the evolutionary model suggests. If I\’m just swapping making point mutations, how can I ever get a new coding sequence?
And for that matter, where do extra chromosomes come from? Why do humans have 46, dogs have 78, horses have 64 and pigs have 38. Aren\’t we all mammals? According to evolutionary theory shouldn\’t we all the same or at least very close-to-the-same numbers of chromosomes? Every case of \"extra\" chromosomes that I have seen leads to fatality or sterility.
@Tom, inbred mice:
I guess my point is that genetic changes are cumulative. If the first mutation of allele X is a simple point site mutation, then of course you won\’t see sweeping changes including entron/exon/codon changes. But if the first change happens not to be a fatal one, it can get passed on. From there, a second or third small change that isn\’t harmful will likewise be coded in the genome and (potentially) get passed on. Ad infinitum. Its the addition of these small changes that creates new functionality over time. IF you can have mutations, AND there is the potential for some mutation not to kill its host, that mutation becomes a vector for change.
But I don\’t really need to even prove that. My first point on your fb page was that there IS a process to make new information. I can change the word CAP to CAT and count that as new information whether the word CAT makes sense for my purposes or not. If we agree that mutations occur at all, then we agree that DNA can change over time.
Secondly, there are ways to create new information besides just swapping out code. Insertion mutations do this. Look at Huntington\’s disease on Chrom 4. This is an insertion mutation that increases the number of CAG repeats apparently randomly. This is another one that is harmful, but that should be expected since most mutations are. Here\’s an example of one that was discovered between a mother and her two daughters
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1288149
For the record, its the number of repeats that causes harm. A normal allele can have anywhere from 11 to 34 CAG repeats, and it can vary widely from person to person. Therefore you can have an insertion mutation that adds CAG repeats to this gene and it will have no apparent effect on its host. Nonfatal mutation.
@Tom, inbred mice:
I guess my point is that genetic changes are cumulative. If the first mutation of allele X is a simple point site mutation, then of course you won’t see sweeping changes including entron/exon/codon changes. But if the first change happens not to be a fatal one, it can get passed on. From there, a second or third small change that isn’t harmful will likewise be coded in the genome and (potentially) get passed on. Ad infinitum. Its the addition of these small changes that creates new functionality over time. IF you can have mutations, AND there is the potential for some mutation not to kill its host, that mutation becomes a vector for change.
But I don’t really need to even prove that. My first point on your fb page was that there IS a process to make new information. I can change the word CAP to CAT and count that as new information whether the word CAT makes sense for my purposes or not. If we agree that mutations occur at all, then we agree that DNA can change over time.
Secondly, there are ways to create new information besides just swapping out code. Insertion mutations do this. Look at Huntington’s disease on Chrom 4. This is an insertion mutation that increases the number of CAG repeats apparently randomly. This is another one that is harmful, but that should be expected since most mutations are. Here’s an example of one that was discovered between a mother and her two daughters
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1288149
For the record, its the number of repeats that causes harm. A normal allele can have anywhere from 11 to 34 CAG repeats, and it can vary widely from person to person. Therefore you can have an insertion mutation that adds CAG repeats to this gene and it will have no apparent effect on its host. Nonfatal mutation.
Duplication adds info to the genome. Quoting Ernst Mayr, “What Evolution Is”:
[quote]Additions to the genome come not only by the duplication of single genes, but sometimes through the duplication of groups of genes, whole chromosomes, and entire chromosome sets. For instance, a special mechanism, involving kinetochores, can lead to a duplication of chromosome sets in certain orders of mammals, leading to highly variable chromosome numbers in these orders.[/quote]
So now I have to google kinetochores (never heard of ‘em) and see how that works, and what mammals are affected =).
@ Tom, oceans and UV post:
OK, I am gonna try to get to the first part of this post later, but to this statement
[quote]Lastly, the modern theory of how information got coded into DNA has us starting with RNA. But RNA is even less stable in water than DNA. If the RNA isn\’t in a perfect salt and pH solution, the water hydrolyzes the RNA… it cut\’s it into pieces.[/quote]
I think you are starting at the wrong end of the puzzle. We cannot begin with fully functional RNA and then add the environment and examine the odds that way. It’s better to start with the environment in which (we presume) the RNA was formed. It makes much more sense that way. It is because of the particular pH, salinity, whatever else of the primordial environment that we have the RNA we see today. Had any factor in the environment been different, we’d be looking at a different product right now, or possibly no product at all. We get what the environment will tolerate and nothing else.
@ Tom, salinity and pH of Oceans:
According to this guy, the oceans are not becoming more salty, and runoff adds only a trivial net amount of salt to the oceans.
http://www.sciencedaily.com/releases/2007/10/071012104955.htm
[Quote]Now, the ocean’s salinity is basically constant. “Ions aren’t being removed or supplied in an appreciable amount,” McKinley says. “The removal and sources that do exist are so small and the reservoir is so large that those ions just stay in the water.” For example, she says, “Each year, runoff from the land adds only 0.00005 percent of total ocean salts.
…
There is geologic evidence that the saltiness of the water has been the way that it is for at least a billion years.[/quote]
Current research indicates that the oceans were formed after millions of years of rain after the earth’s crust solidified (saw it on How the Earth Was Made on the History channel, which was awesome). It did not bubble up from the core, and there’s too much for it to have leached out from gas vents in the mantle. What that means is that the same earth from which salt is now leaching was the earth the oceans were first formed on, making it virtually impossible for the ancient oceans to have been freshwater. They were saline.
And the pH delta you cite is the result of human activity:
http://en.wikipedia.org/wiki/Ocean_acidification
Therefore, you can’t extrapolate that backward more than a few centuries at best. It’s a very recent trend, not one our single celled ancestors had to worry much about.
OK. Rather than deal with citations from competing experts let\’s pick a simpler topic where there is not a lot of room to call on experts. I don\’t think any good comes from a battle of competing experts on topics like this.
If evolution from single-celled to advanced organisms is true then there is an entity called the Last Universal Common Ancestor (LUCA… or some places call it LUA and leave out \"common\"). LUCA represents the core functions and genes that had to be in place before the major divisions of cell types happened (Prokaryote, Eukaryote and Archaea).
http://en.wikipedia.org/wiki/Last_universal_common_ancestor
Once of the many characteristics of LUCA is that all amino acids used in protein synthesis of in the L-form.
L and D are the 2 forms of enantomers. Enantomers are chemically identical, they just have a 3-dimensional shape that is mirrored. They have the same bond energetics. They have the same chemical makeup. They react identically in every chemical situation not regulated by enzymes (because enzymes work based on 3-dimensional fit).
When derived from non-enzyme reactions, amino acids form the L and D form equally, 50% L and 50% D. Even if they aren\’t perfectly 50/50, the problem described below is the same.
Here is the issue. The LUCA uses only L-form amino acids for all 20 amino acids in all steps of protein synthesis (one D form, D-serine, is used as a neurotransmitter, but is not involved in any protein synthesis). But why the L-forms? Although there is a free-energy advantage to using a pure L or D form, there is no advantage to using L instead of D. Thus, random evolutionary processes had to select the L form for every amino acid. But that\’s not the real problem. The real problem is that all the enzymes used to build proteins from amino acids had to evolve to use only L form amino acids prior to the LUCA. Let\’s take a look at them:
-The enzymes that synthesize amino acids had to randomly produce all L form.
-The enzymes that link amino acids to tRNA had to randomly evolve to link only L form to tRNA and thus \"charge\" them.
-The enzymes that code for the ribosomal super-structure (over 50 proteins and enzymes) had to randomly evolve to fit only L form amino acids in the synthesis machinery. Some D forms are lethal because they stop protein synthesis here.
-The enzymes that function as elongation factors (like peptidal transferase) had to randomly evolve to make peptide bonds only for L form amino acids in elongation.
So what are the odds of this happening by random mutation? I\’m not talking about the random development of the genes that code the proteins, I am only talking about just getting the L form for every amino acid instead of having a mix of L and D forms.
Since there are 20 amino acids and each could be either L or D, that gives us a 1 in 2 to the 20th power or 1:1,048,576 or ROUGHLY 1 IN A MILLION FOR EVERY PROTEIN/ENZYME IN THE PROTEIN MANUFACTURE PROCESS THAT HAS AN L FORM DEPENDENCY FOR AMINO ACIDS.
If I assume that that there is only 1 protein/enzyme per above process that was L form dependent (BTW – that is WAY understating it), then I get a chance of pure L form selection occurring by random evolutionary processes as 1 in 2 to the 80th, or:
1:1,208,925,819,614,629,174,706,176
To put that in perspective, if you have a thousand random mutations a second it will take over 38 trillion years to achieve an all L form instead of some mix of L and D form.
The prevailing model of the age of earth at about 4.5 billion years old. Stromatolite (fossilized cyanobacteria mats) are the oldest demonstrable life and date conservatively at 2.7 years old and strong evidence for an older stromatolite dates at 3.5 billion years old. Cyanobacteria are photosynthetic and since photosynthesis is not part of the LUCA, then the LUCA has to be older than the cyanobacteria. The LUCA is estimated around 3.8 billion years ago for this reason. If it took 300 million years for the earth to cool enough for life to start to form, then you essentially have .5 to 1 billion years to go from no life to the LUCA.
The next thing to consider is that all the really fast methods of adding DNA to a genome come from mechanisms that themselves had to evolve after the LUCA since they are all tied to chromosomal mechanisms like recombination (crossing over) and chromosomal duplication. Since chromosomes are not part of the LUCA, they had to evolve afterward. This leaves pre-LUCA evolution to rely essentially on point mutation, frameshift mutations and other DNA mutations that have a tiny impact on DNA elongation. This is consistent with the fact that the cambrian explosion of diversity and species is about 3 billion years after the LUCA. Evolution proceeded rather slowly prior to the cambrian explosion.
Putting all this together, the exclusive use of L-form amino acids (called homochirality) in early stage evolution is statistically impossible. The evolutionary model requires too much functionality too early on. Logically, this only leaves 2 other options: intelligent design and exogenesis (the idea that earth was seeded from outer space). The weight of evidence against exogenesis is considerable and most people consider it to be a far reach. Intelligent design is picking up a lot of ground in many distinct science disciplines from geology to astronomy to biology. I believe that the affirmative case for intelligent design is compelling but that is a bit beyond the case of micro and macro evolution as is set forth in this thread.
OK, Real Madrid is here playing DC United today, and I have to leave for that soon, so I’ll be getting back to you. I was looking at your LUCA and thermodynamics entry, so sometime this evening I should be posting a response to both.
What experts are you citing, tho? The Huntington’s stuff I cited, for example, is pretty incontrovertible given that we can actually scan their code and establish with finality that an insertion mutation occurred. So is this the salty oceans one or the pH one? I’m dropping it, its just I’m surprised because I looked at more than one source and didn’t see a lot of disagreement. I’ll google it again, tho.
Quickly, tho, how are you getting 1:1,208,925,819,614,629,174,706,176? How is it 1 in 2^80? I see the 1:1,048,576.
later.
Your huntington citation is solid. It is clear that DNA elongation is taking place there. In fact I spend a good deal of time looking into the entire field of DNA mutations because of this reference. Here is a quick summary of what I found regarding DNA mutations:
1 – DNA mutations can be broken into two large groups. Those caused by environmental factors (UV, oxidative damage, tautomeric-based mutations, etc) and those caused by enzymatic activity (issues with recombination/crossing-over, antibody active site recombination, etc).
2 – Bacteria have circular DNA with only a single copy. When mutations happen they are incorporated very quickly because they don\’t have a second copy of the DNA like eukaryotes usually do (for example, humans have 2 copies of 22 chromosomes then the X and Y chromosome make 46 total). Also, prokaryotes (like bacteria) don\’t tend to have \"junk\" DNA like eukaryotes do. So if you have a mutation in prokaryotes, it is much more likely to occur in a coding sequence. A consequence of this is that bacteria have a hard time adding DNA new coding sequences from environmental factors (I\’m talking about DNA elongation). Most cases of net new coding sequences through DNA elongation that occur in bacteria happen due to (1) retroviral activity, (2) gene transfer, or (3) transformation (where a cell uptakes and incorporates DNA from outside the cell… most bacterial factories operate this way). All three of these forms of bacterial DNA elongation depend on very sizable protein and enzyme complexes. Those protein/enzyme complexes had to evolve before they could be a basis of DNA elongation in bacteria. When you look at the world of DNA mutations that are possible prior to the evolution of these protein/enzyme complexes, you lose a lot of speed. The only form of environmental-only DNA elongation that I can think of for bacteria is a frameshift mutation that slips backwards, thus elongating the daughter strand. But I haven\’t seen any evidence of this kind of frame shift, it just seems theoretically possible to me. Thus when when we look at bacterial DNA elongation in the evolutionary timeline, the elongation had to start with environmental factors only and eventually evolve the protein/enzyme complexes that allow modern elongation to take place (through bacterial conjugation, retroviral action, transformation, etc).
3 – When we look at DNA elongation in eukaryotes we find a similar state as prokaryotes, but with some meaningful differences. DNA elongation in modern day eukaryotes can happen very rapidly BECAUSE OF the protein enzyme activity at play acting specifically on DNA (recombination/cross-over, meiosis, etc). DNA in eukaryotes also has the ability to do chromosomal duplication, but these too are a function (or error in function) of massive protein/enzyme systems (for example, a failure in meiosis creates gametes that lead to Downs Syndrome and Trisomy). Eukaryotes have lots of junk (non-coding) DNA which in my mind gives them a massive evolutionary advantage over prokaryotes because mutations aren\’t nearly as likely to cannibalize 1 gene to evolve a new one (like would need to happen in must higher frequency prokaryotic evolution). But with regard to eukaryotes and DNA elongation, all the factors that allow the elongation of modern eukaryotes, had to evolve. In addition, telomerase is not part of LUCA so telomerase had to evolve after basic DNA replication evolved. Telomerase puts repeating sequences of DNA at the end of straight DNA sequences. The problem that telomerase fixes that straight DNA replication cannot copy 100 percent of the strand so with each replication you lose a few DNA bases off the end. So in early evolution of eukaryotes, you have to rely on environmental elongation only AND it has to elongate faster than the net loss of DNA due to lack of telomerase.
So my argument changes a bit from what I first hypothesized. At the outset of the discussion my claim was that species were formed by a sub-speciation process through allele loss for a polymorphism. Or in other words, my own variant of microevolution.
Now, I recognize the possibility for the modern genenome to accumulate new genes by DNA elongation and mutation of existing sequences, but all those mechanisms that allow new genes to form seem dependant on protein/enzyme complexes that themselves have to had evolved. Thus we have another chicken/egg problem. Which came first: DNA elongation or the protein/enzyme complexes to allow DNA to elongate? These kinds of problems in evolutionary mechanisms point to strongly to design.
BTW – the competing experts issue that I have is surrounding early earth conditions. There is too much variability in the field to try to pin-down any definitive early earth conditions. So when we talk about how an RNA world could have existed, I am OK with plausibility models. But when a plausibility model has viable and mutually exclusive competing models, then we have to say that we don’t know enough about the starting conditions to launch a debate. You say that ocean salinity is contested: it is. Both models can’t be right and both models have decent data and arguments. RNA world has meaningful and serious competitors as a plausibility model. To that end, I say, let’s not debate in this area where there is such an absence of data.
The Last Universal Common Ancestor (LUCA) on the other hand, is a logical imperative of evolutionary theory. As such we can rely on logic and reasoning to make arguments and don’t necessarily have to engage topics like RNA world.
As for the calculations to come up with 2^80.
I cited 4 distinct protein/enzyme complexes in the protein synthesis process.
Complex 1 – creates L form only amino acids
Complex 2 – attaches L form amino acids to a tRNA
Complex 3 – Ribosomal framework that decodes the mRNA and that fits only tRNA complexed to L form amino acids (incidentally, some D form amino acids are toxic. I am trying to find out why they are toxic. The best I can find so far is that it looks like the toxic D form amino acids lock-up the ribosomal framework similar to antibiotics like erythromycin… I’m still working on this one)
Complex 4 – protein elongation by forming peptide bonds between the L form amino acid and the portion of the protein in front of it.
Since each protein sequence requires that a DNA coding sequence randomly evolve to produce it, then each protein segment or complex of proteins that works only with L form amino acids becomes an independent member in the probability calculation. When probabilities are independent, then you multiply them to get the total probability.
I don’t actually know how many independent proteins are L-form specific in each complex, so I went with the lowest possible number per complex: 1. If other protein segments within a given complex are also L-form specific, then the number of independent variables in the probability increases.
If the probability of 1 complex using only L form amino acids is 1:2^20 (or 1:1,048,576), then the odds of all 4 protein complexes randomly and independently evolving L-form specificity is multiplicative: 1:2^20 x 1:2^20 x 1:2^20 x 1:2^20 –> or –> 1:2^80 –> or –>
1:1,208,925,819,614,629,174,706,176.
It’s worth noting that since some D forms are toxic, then we might need to add a 5th complex to the probability equation to factor for purifying any mixing of L and D forms inside the cell (currently done by enzymes called racemase). If that turns out to be the case, then the minimum probability goes from 1:(2^20)x4 to 1:(2^20)x5 or 1:2^100 or:
1:1,267,650,600,228,229,401,496,703,205,376
Tom,
Still working on earlier posts of yours, but quickly, you said this
[quote]Which came first: DNA elongation or the protein/enzyme complexes to allow DNA to elongate? These kinds of problems in evolutionary mechanisms point to strongly to design.[/quote]
I know this one off the top if my head (mostly because I’ve been refilling it with all my old bio and genetics texts thanks to all the homework you’re giving me these days
). The DNA elongation came first because they don’t need enzymes to replicate under the right conditions.
The nucleotides that make up DNA are relatively stable, but can be denatured with heat from an external source. Once a polynucleotide strand is denatured from its compliment (unzipped from the helix), it serves as a template for a new DNA strand by bonding with other free nucleotides. It can match with other single units or strands of units, and it can pair with them in a way that leaves unpaired units on either end that can cause a longer paired strand that it started as. For example:
Say we have this paired sequence on the left. Add heat and we get two unpaired sequences:
CCTGG + heat = CCTGG and GGACC
GGACC
These unpaired sequences are now floating in a sea of other nucleotides, which we have established can form under natural conditions abiotically (see Miller-Urey http://en.wikipedia.org/wiki/Miller-Urey_experiment ).
Now suppose that in this warm soup of nucleotides, they rebond together (or with a different strand with complimentary units, doesn’t matter), but unevenly:
CCTGG
CCAGG
now if other strands or singletons in the soup bond on the loose ends, you will end up with a longer strand than you started with using no replication enzymes whatsoever. And every time a coupled unit gets denatured, its another chance to reproduce using itself as a template. Voila, DNA elongation came first.
crap, the html took out my spaces in the example above. The last strand pair in the above example should be this:
CCTGG…
…CCAGG
with the periods replacing spaces. You get the idea.
Concerning the 2nd Law of Thermodynamics…are there not violations of the 2nd Law present in nature? The 2nd Law of thermodynamics is dependant upon equilibrium…for instance; what happens when the heat from a warmer body dissipates naturally to a cooler body? Over time, and as the temperature of both bodies equal one another…equilibrium is achieved. If this is the case, how can the entropy of the universe continue to increase if no verifiable changes are occuring because of a state of equilibrium?
@Tom, 2^80:
OK, That’s a start. I’ve been looking into several issues here and I see some loopholes. First, if we are looking at enzymes that create L form amino acids in humans, for example, we are actually only dealing with the 12 enzymes that create the *non-essential* ones and that’s because human’s can’t synthesize all amino acids (AAs for short). We get the remaining 8 in our diets. So just for humans, your figure drops from 1 in 2^20 to 1 in 2^12.
I mentioned in an earlier post, amino acids are readily available in the primordial environment from inorganic processes consisting of water, methane, ammonia, and hydrogen. So its possible for organisms prior to LUCA to have begun without the ability to synthesize ANY of these AAs. I don’t have the foggiest idea how many LUCA could synthesize, but it is at least possible that it didn’t have to make them all.
But lets say LUCA needed to synthesize all the AAs. There’s another issue, one I brought up before. Genetic changes are cumulative, and their diversification grows like a tree’s branches. What that means here is that the enzymes we are considering for each set of your complexes are related, born out of the same duplicative processes we’ve already discussed. Each one need not, and in fact wasn’t, arrived at from scratch as your 2^80 figure implies. tRNA, for example, in Eukaryotes has some 32 versions for the 20 AAs we are dealing with. But all of those versions has the same base structure, and in fact all tRNA in all species on Earth shares this base structure because they all derive from some proto-tRNA code with that structure, which need only have evolved ONCE. So if that initial structure was of one chirality and was the base for all the others, it means that the chirality was not a 50/50 probability but rather was selected early on and passed down through all successful variants in that complex.
The complexes themselves are also related through RNA. If the enzymes require a particular chirality of the AAs to work, code for enzymes of that chirality evolving in the RNA will be more successful. Once in the RNA, it can be duplicated in code for the chirality of tRNA, and mRNA, which is a direct copy of RNA in any case, and in the ribosomes as they evolve and be passed through those complexes. So it may not be as random as it appears in the formula. Once a chirality is selected, the odds of it cropping up in other enzymes is greater than 50% due to inheritance.
@Tom. Another question. In your post a few days ago, you mention that LUCA can’t derive energy from the sun without using photosynthesis, but in the wiki link you posted it says clearly that LUCA derived its energy from glucose via glycolysis. Maybe I’m missing something, but how is this a problem? Is it a problem?
Autumn, regarding DNA elongation in the primordial soup.
quote:
“Say we have this paired sequence on the left. Add heat and we get two unpaired sequences:
CCTGG + heat = CCTGG and GGACC
GGACC”
Yes, you can heat DNA to cause the strands to separate and yes, it can re-anneal due to the action of hydrogen bonding. But this doesn’t produce elongation because you are not making new phosphodiester bonds between the base pairs. The phosphate group that makes the linkage is not part of the DNA bases prior linking into a DNA strand.
Furthermore, and more importantly, These phosphodiester bonds can only be formed by enzyme activity. Even in Polymerase Chain Reaction (PCR) which is the lab method for DNA replication, you have to use the enzyme Polymerase.
Here’s another plug for Wikipedia:
http://en.wikipedia.org/wiki/Phosphodiester_bonds
Autumn, regarding Miller-Urey and pre-biotic conditions.
The Miller-Urey experiment (and all similar experiments) use reducing environments and high-energy sources to produce amino acids and a few other organic molecules. In Miller-Urey specifically, they used high voltage electric sparks. This is needed because it is the energy source for the creation of the new chemical bonds in this environment.
There are 3 major problems with using Miller-Urey type reactions as the basis of DNA elongation:
1 – Miller-Urey type reactions don’t produce any nucleotide molecules (the building blocks of DNA and RNA) or anything close to them.
2 – The phosphate ion needed to produce the DNA phosphodiester bond is acidic and would wreck the reducing environment requirement for the soup.
3 – These reactions are pre-biotic. Once you have cells, even the most basic ones, then you have to turn-off the lighting or you destroy the cell. Therefore, even if a pre-biotic environment could produce small DNA sections, it would not be able to be part of the chemical elongation inside the cell or else it would destroy the cell.
Autumn, regarding the improbability of evolving L-form AA dependent protein/enzyme complexes.
Essential/Non-essential would not reduce the probability from 2^20 to 2^12 because all 20 amino acids are synthesized in the biota as a whole. So even if humans don\’t synthesize proline, some other organism had to develop a L-form dependent synthesis apparatus. Thus, because all 20 are formed somewhere in the biota, the number remains 2^20 for the L-form synthesis step.
Even if LUCA didn\’t synthesize all 20 amino acids, it would still have to have receptor-mediated cell-surface protein-based active transport of L-form amino acids to the inside of the cell. In essence, it had to make or specifically eat all 20 L form amino acids. Whether the L form specificity is in manufacture or receptor based down modulation, the sourcing of L-form amino acids still remains 2^20.
As for tRNA structure commonality, tRNA isn\’t a protein and isn\’t built of amino acids. My probability model is based on the protein/enzyme complexes that bond a specific tRNA to a specific L-form amino acid. That enzyme complex that links them is what I am talking about. So what about common structure ancestry to this enzyme/protein complex? Here we have 2 potential competing factors that affect the 2^20 probability.
On the reducing side (lowers the probability of 2^20), we have what you spoke about. Commonality and genetic inheritance of the tRNA-L-form-AA binding complex components. However, I don\’t accept it 100% the way you describe because there is a race condition at play here. Until you can actually make proteins, the DNA that codes for this complex must develop completely randomly because DNA copy requires proteins and enzymes: environment only produces point mutations. In essence, it would be useless until it was minimally functional to produce copied sections of DNA as the basis of copy-able commonality. So it would have to randomly evolve minimal protein synthesis functionality necessary to copy DNA before any common code inheritance could occur. Let\’s say that minimum functionality involves 15 of the 20 amino acids. If that was the case, then 2^20 would reduce to something like 2^15 plus remaining probability of the remaining 5 dependent variables (something like 2^15 x 1.25^5).
On the other hand, a competing probability factor to drive the probability up above 2^20 is the fact that there are not just 20 tRNA… there are at least 64 at LUCA. Why? Because the genetic code is set by the LUCA arrives. The code is a base sequence, but there are 4 possible bases in each of the 3 spots. Thus there are 4^3 or 64 codons. By the time LUCA is present all 64 codons code to 1 of 20 tRNA anti-codons. Thus the tRNA-AA binding complex actually has to specifically bind 64 distinct pairs. The probability due to this combination would go up as high as 2^64.
The real answer for the tRNA-L-form-AA binding complex having L-form specificity for all 20 amino acids is going to be somewhere between the minimum functional protein synthesis model number (I used 15, so 2^15) and the number of tRNAs that code for a specific L-form amino acid (2^64).
Lastly, chirality transfer from RNA to AA has things backwards. The DNA has to code for the manufacture of a left-handed glove before you can fit a left-hand into it. All these protein complexes that I\’m talking about are left-handed gloves. Chirality transfer from RNA would be the similar to me putting a left-handed glove on my right hand and the thumb of the glove magically changing to fit my hand. In the enzyme-substrate model you make a glove and you have a hand and if they don\’t fit, they don\’t change to fit. You can have chiral transfer from some amino acids to others under special conditions. But since the mandate in LUCA is DNA to RNA to protein, the only way to change a right-handed glove to left-handed is to change the coding sequence of the DNA. Thus RNA cannot transfer it\’s chirality to the protein complex of the ribosome.
@Tom
1. See “Other experiments” under Miller Urey.
[quote]Experiments conducted later showed that the other RNA and DNA nucleobases could be obtained through simulated prebiotic chemistry with a reducing atmosphere.[/quote]
2. Not sure what you mean here. The environment for the soup was free of oxygen, true, but phosphate in solution doesn’t yield O2. The phosphate ion PO4 hydrolyzes in water like this:
PO4(3-)(aq)+ H2O(l) HPO4(2-)(aq) + OH-(aq)
The hydrogen phosphates likewise produce H2PO4 or H3PO4 and hydroxide. They do not release O2 and therefore do not oxygenate the soup. And the resulting phosphate ions (PO4, HPO4, H2PO4, and H3PO4) are all present, and represent a range of pHs, where phosphoric acid (H3PO4) is acidic, true, but H2PO4 can react as an acid or as a base, for example. The acidity depends on the ratio of each of the products in the solution.
3. Correct. This is not part of any cellular process, but it is a pathway for DNA elongation without enzymes, which was my point. Elongation is possible before the evolution of any complex structures for translation, repair, or even for cell membranes. It’s therefore possible that the code for primitive versions of these structures was arrived at before they were wholly necessary. Doesn’t get me far as to the how the first cell accomplished the task since this area is so hypothetical, but its a more or less plausible answer to your chicken and egg point.
Autumn,
I officially have no life now
)
Regarding Miller-Urey type reactions:
1. A nucleobase is not a nucleoside. A nucleobase is the purine or pyrimadine ring structure portion of a nucleoside. A nucleobase is much simpler than a nucleoside. A nucleoside is a nucleobase and a sugar bound together in a specific way (Ribose for RNA and Deoxyribose for DNA).
The conditions needed to produce nucleobases are pretty impressively complicated. But the prebiotic conditions necessary to make and sustain ribose are just about impossible because the reaction chamber needed to create ribose is the same reaction chamber that destroys it. Here is a Harvard abstract describing the problem in prebiotic ribose synthesis:
http://adsabs.harvard.edu/abs/1988OLEB…18…71S
2. All pre-biotic reaction scenarios require a reducing environment as it relates to Oxidation-Reduction (aka Redox) reactions. Phosphates exist as salts or acids. Either way, the phosphates have an oxidizing (but not oxigenating) affect on their environment. This oxidizing effect is a function of electron flow, not oxygen flow.
3. Your hypothesized plan requires prebiotic DNA formation and prebiotic phosphodiester bond formation between the DNA molecules. Then, once the short segments pair-up in their hydrogen bonding and anneal, you have to create phosphodiester bonds between the unlinked DNA pieces while they are hydrogen-bond complexed. In modern genomes DNA ligase would do this function. But since prebiotic DNA elongation would need a ligase function and because the DNA ligation points are spatially blocked by the surrounding hydrogen bonds, and upstream and downstream DNA, then clay substrates and other such environmental enzymes would not be able to get to reach the ligation point and help the formation of the phospodiester bond. Therefor, if you cannot create phosphodiester bonds predictably, then you cannot elongate DNA.
Autumn,
You asked this question several posts back. Here is your question:
—-begin quote—–
Another question. In your post a few days ago, you mention that LUCA can’t derive energy from the sun without using photosynthesis, but in the wiki link you posted it says clearly that LUCA derived its energy from glucose via glycolysis. Maybe I’m missing something, but how is this a problem? Is it a problem?
—-end quote——
Glycolysis is the extraction of energy from glucose. What is the ultimate energy source for all glucose formation? The sun through photosynthesis.
LUCA uses energy from glucose. But photosynthesis had to evolve after LUCA since it is not part of LUCA. And it had to evolve really fast. From LUCA to cyanobacteria is about 300 million years.
Thus we have a case where the evolutionary implications has produced events that could not have happened according to the data. More specifically, that glucose metabolism (glycolysis) evolved before glucose production (photosynthesis).
@Tom, phosphodiester bonds
[quote]These phosphodiester bonds can only be formed by enzyme activity. Even in Polymerase Chain Reaction (PCR) which is the lab method for DNA replication, you have to use the enzyme Polymerase[/quote]
No, that\’s not how chemistry works. There is no such thing as a chemical bond that requires an enzyme to happen. Enzymes are there to control the reactions so they happen in a predictable manner, location, and time. The chemistry of the bond itself needs nothing but opportunity, time, and energy. The enzyme is the most efficient way we know to do it, but it isn\’t required. They use them in labs because getting a .05% success rate may not suit their ends or their budgets, but that doesn\’t mean there is something special about the bond that only an enzyme can achieve it.
@Tom, photosynthesis and glucose
[quote]Thus we have a case where the evolutionary implications has produced events that could not have happened according to the data. More specifically, that glucose metabolism (glycolysis) evolved before glucose production (photosynthesis).[/quote]
No, I don’t think that’s right. We know that we can get amino acids naturally from the Miller Urey experiment. If you read it, you see that we ALSO get sugars. See the text under Experiment and Interpretation:
[quote]At the end of one week of continuous operation, Miller and Urey observed that as much as 10–15% of the carbon within the system was now in the form of organic compounds. Two percent of the carbon had formed amino acids that are used to make proteins in living cells, with glycine as the most abundant. Sugars, lipids, and some of the building blocks for nucleic acids were also formed.[/quote]
Sugars were there in D and L form, waiting to be consumed by whatever metabolic process existed. Which makes sense, LUCA would not have gotten off the ground as a concept if such a simple omission could derail it.
[quote]A nucleobase is not a nucleoside. A nucleobase is the purine or pyrimadine ring structure portion of a nucleoside. A nucleobase is much simpler than a nucleoside. A nucleoside is a nucleobase and a sugar bound together in a specific way (Ribose for RNA and Deoxyribose for DNA).[quote]
Well, its not that much simpler. The difference is the phosphate group, the PO4. That’s not much except that we disagree that PO4 can exist in the environment without destroying the environmental conditions for the nucleotides.
And @# 2, your term threw me off. We are talking about two different things. A reducing environment is also one in which there is little or no free O2, which is relevant because O2 can terminate abiogenesis. Which is what set me down the wrong path.
OK, so if the soup was also reducing in terms of redux reactions, there still isn’t any problem with having phosphate in the system. A reducing environment does not prevent phosphate or its related compounds, and simply having phosphate can’t destroy the environment.
[quote]Essential/Non-essential would not reduce the probability from 2^20 to 2^12 because all 20 amino acids are synthesized in the biota as a whole. So even if humans don’t synthesize proline, some other organism had to develop a L-form dependent synthesis apparatus. Thus, because all 20 are formed somewhere in the biota, the number remains 2^20 for the L-form synthesis step.[/quote]
I think we are missing each other. Not being able to synthesize an AA does not preclude you from using it as long as that AA exists in your environment, and we have established that AAs can be generated through non-biological processes, not just from biota. I used humans as an example of an organism that requires externally generated AAs to show that in the place of LUCA, we can still theoretically get all 20 AAs even with an impartial synthesis mechanism. LUCA need not have a complete array of AA generating enzymes in order to use those AAs.
I’ve been reading all of the post for some time now. I can say, I am no geneticist; however, I do understand enough to follow along. I’ve known Tom for quite some time and count him among my best friends. Man, all of the discussion on this post leads me to only one conclusion; there are high levels of organization occuring in the primordial ooze. Concerning the 2nd Law of Thermodynamics, we know that in closed systems things move to a greater state of entropy. Furthermore, when equilibrium is achieved, as is occuring in all systems, we reach a state called maximum entropy. The eventual end, as scientist refer, is called Heat Death. Entropy, by definition, is an increase in the randomness of the universe, until we reach equilibrium and no further energy is exchanged, either on the molecular level, or a system level in general. It appears, at least to me, high levels of organization run counter to the teachings of the 2nd Law. We know there are ways to decrease the randomness of the universe, ie; frictionless adiabatic compression, but scientist have not been very succesful at either creating a natural environment where this occurs, or discovering it in nature, or admitting that the 2nd law has major flaws. I guess the question I have is; if we are to believe organization of this magnitude on a genetic level occured spontaneously…what are the odds. As Einstein would say, “God is not merely out there rolling the dice.” High levels of organization do not verify or support the idea of entropy and the 2nd Law. Boltzman, Planck and Einstein all recognized, through study, that the universe was highly organized, which led to some of the greatest doubts and concerns concerning the 2nd Law. Please advise and educate or correct at your leisure.
@Charles
Interesting. It seems that part of what you are getting at is that all life violates the 2nd law of thermodynamics. Well, what does the 2nd Law say? It says that entropy will tend to increase. It does NOT say that a localized system can’t decrease in entropy at the same time, just that the aggregate of open systems must show an increase, however gradual. An open system is any system that can communicate energy or material in or out of it.
High levels of organization are rarer than you might think. We may think of a planet as organized because it is a nice rounded unit of material floating in a less organized space, but think of it this way: how many planets are there that are made entirely out of super complex units like rabbits? I mean the whole planet. No ocean, no crust or mantle, no dirt or sand or Starbucks, just rabbits on top of rabbits.
Through the lens of entropy, that’s impossible because a complex, low entropy open system like a rabbit requires high entropy from another system to drive it. While the vegetation it eats are low entropy like the rabbit, they require the energy and material from simple disorganized, high Entropy earth to grow in and enough of that to provide gravity to keep them reasonably attached. And high entropy bodies of water and weather to disperse and hydrate them. And high entropy UV radiation from the sun so the plants will grow. And a high entropy atmosphere for respiration, etc, etc. You end up with a sizable planet of mostly dirt, water, air, and some vegetation on the outermost crust just to support a single rabbit. That’s a huge amount of high entropy supporting very, very little low entropy.
So while the universe can be argued to look highly organized, compared to a living organism it simply isn’t. There will always be more high entropy than low because the energy it provides drives the uphill complexity we see in living organisms, and therefore there’s an upper limit to the number of rabbits but no lower limit, so high entropy always wins in the end. So until there are low entropy increases that result in more rabbits by volume than stars, planets, and black holes, I think the 2nd Law should be safe.
One of the difficulties of talking about the origins of cells and the feasibility of evolution is that we very often mix prokaryotic and eukaryotic features in thinking about early cells. And I can certainly understand why we do that… we don\\\’t know which was first: prokaryote, eukaryote or archaea. Let\\\’s simplify it a bit, we don\\\’t know if the first DNA was straight (like eukaryotic) or circular (like prokaryotic).
If you try to defend straight DNA as the first, you run into lots of problems like sticky ends, frayed ends, the fact that replication enzymes can\\\’t actually copy a whole strand of straight DNA (the enzymes have to attach a couple of bases from the beginning and drop off a couple of bases from the end… so you lose about a half a dozen bases on each replication). The problems with straight DNA as the first form are more or less insurmountable.
Now what about circular DNA? It has other problems. For example, primordial circular DNA would not be able to elongate since all circular DNA elongation is a function of enzyme activity of things like retroviruses. Another problem with circular DNA is that the first circle has to first be straight and short, then a phosphodiester bond has to form between the two ends of the short DNA strand.
When talking about the early genome we sometimes say that the first DNA was circular (prokaryote only) so as to be stable and then say DNA elongation happened by errors in recombination (eukaryote only). This kind of mixing of mechanisms confuses the analysis of feasibility of early evolution.
Earlier, we spoke about the Last Universal Common Ancestor (LUCA). Since the evolutionary model starts with one cell and becomes increasing more complicated, the idea of LUCA is mandated by logic. The features of LUCA are those that are common to all cells like:
1. DNA is made of the 4 bases abbreviated A, T, C, and G.
2. Proteins are the functional bodies withing cells and special forms of proteins called enzymes catalyze reactions.
3. DNA to RNA to protein as the central dogma of biology
4. 20 amino acids out of innumerable others make the basis of all proteins and all these amino acids are in the L form.
5. ATP is the energy source that drives virtually all enzymatic activity in the cell
6. cells multiply by duplicating all its contents, then dividing.
Why I mention this is because a logical requirement of LUCA is that one form of DNA (either straight or circular) had to get the process of evolution from a single cell all the way to LUCA all by itself. If it didn\\\’t, then it would not be the last universal common ancestor.
The age gap between LUCA and the oldest known cell (cyanobacteria) is about 300 million years (very short time in the time-line of evolution). Cyanobacteria are prokaryotic. LUCA is not photosynthetic. Therefore if LUCA had circular DNA, then only photosynthesis had to evolve in those 300 million years but the DNA could not elongate by any reasonable means because that is not what circular DNA does. However, if LUCA had straight DNA, then a circular DNA form had to evolve in addition to evolving photosynthesis and in addition to a selective loss of non-coding junk DNA that seems to be inherent in straight DNA.
When you apply this logical requirement (that DNA had to either be straight or circular) to all cell forms leading to LUCA, then we find that neither one really can stand.
Autumn,
The chemistry of Polymerase Chain Reaction (PCR) seems to have caused us some difficulty in our discussion. My claim is that the phosphodiester bond that becomes the backbone of a DNA strand is not easy to produce.
Let me start with a discussion of nucleobase, nucleoside, and the 3 types of nubleotides (monophosphate, diphosphate and triphosphate).
A nucleobase is a purine or pyrimidine ring structure that is 1 of 3 core components of the DNA nucleotide makeup. This is the only piece of DNA that has been synthesized in reactions like Miller-Urey.
A nucleoside is a nucleobase plus a sugar. DNA uses the sugar deoxyribose. RNA uses the sugar ribose.
Lastly, a nucleotide is a phosphorylated nucleoside. There are mono-, di-, and tri-phosphate nucleotides. In a DNA strand, the mono- form of C, G, T, and A are found. For example, Adenesine monophosphate (AMP) is a component of DNA while adenesine triphospate (ATP) is not. As far as bond energies go, nucleoside monophosphates don’t have a lot of free-able energy compared to the di- and tri-phosphate forms.
In polymerase chain reaction (PCR) the recipe requires that your building block nucleotides are the tri-phosphate form (ATP, GTP, CTP and TTP). The monophosphate form becomes part of the newly formed DNA strand, while 2 phosphate ions are given-off for every nucleoside monophosphate that is attached as the DNA chain grows.
The enzyme polymerase consumes the high-energy of the 2 phosphate-phosphate anhydride bonds as the source of the energy to create the phosphodiester bond needed for DNA chain elongation.
PCR will NOT WORK if you only put the mono-phosphate forms of the nucleotides in the reaction vessel because the DNA elongation of the replicating strand through the polymerase enzyme is energy consuming. It takes a lot of energy to add 1 member to a replicating DNA strand.
If we extrapolate this fact to early form DNA, you find that you have to be able to channel a lot of energy from somewhere into the phosphodiester bonds that are the links in the DNA chain. Modern cells use mostly glucose metabolism to create the ATP, CTP, GTP and TTP necessary to replicate DNA AND they have to use enzymes that link them on the 3 and 5 locations of the 5-member deoxyribose sugar. if they link to say, the 2 location instead of the 3, then no DNA as we need it. Linking in somewhat random locations would be what happened if chemical reactions without enzymes were the basis of these reactions.
There is a raging debate in the evolutionary world about what had to be first: metabolism or genetics. In the example that I describe for PCR, we see that picking either first is impossible. DNA replication requires metabolism (consumption of ATP, GTP, CTP or TTP to add a single monophospate member to a replicating DNA strand) AND genetics (the genetic code to code for the enzyme to hook the AMP, GMP, CMP or TMP into the right 3 and 5 positions on the adjacent deoxyribose).
There is one more problem with using systems like PCR as an example of how early DNA could be copied. PCR has a designed component to it which is not allowed according to the rules of evolution. PCR does not work without the use of a primer strand.
Oddly enough, in order to use PCR to copy the DNA that you want copied, you have to manufacture a primer specific to the strand being copied. A primer is a short section of DNA that is complementary to the tail end of a DNA strand and serves as an attachment basis for the polymerase enzyme.
Without a primer, the polymerase cannot latch-on to and copy the DNA strand. No primer, no PCR. Oh, by the way, you need a primer for each tail-end which is almost never the same sequence. Thus you need two uniquely matched primers to allow for polymerase attachment and replication of the template strand.
More homework? OK, I need some time for these, be back later.
But just to get a sense of where we are, it looks like we have agreed that DNA, once established, can elongate, can introduce new code, can change radically after many generations, correct? This is the thrust of the original post by Slugsie, which we have not spent much time on between us. So I am wondering now if you accept evolution post LUCA, because it seems to me that the primary issue we are dealing with here is the pre-LUCA evolution of DNA and DNA replication itself, which is admittedly sticky. Is this correct?
But to the DNA issue, based on my readings last week, we are looking most likely at an RNA origin for these, but the origins even from there are hypothetical and uncertain. They are absolutely not impossible as far as anyone can tell, but the exact mechanisms are not known yet. I’ll do what I can to explain what I have understood of that later.
Tom, phosphorylation
[quote]The conditions needed to produce nucleobases are pretty impressively complicated. But the prebiotic conditions necessary to make and sustain ribose are just about impossible because the reaction chamber needed to create ribose is the same reaction chamber that destroys it. Here is a Harvard abstract describing the problem in prebiotic ribose synthesis[/quote]
Correct, but this is back in 1988 using only formaldehyde as base material, which has since been ruled out as a likely starting point for carbohydrate synthesis. They are currently (since 94) looking at borate minerals, among others now. There have been some tests demostrating that ribose can be synthesized more reliably with that with a lifecycle as long as eight months.
http://74.125.93.132/search?q=cache:Op5XwaHGBbgJ:www.ffame.org/sbenner/science303.196-196.pdf+borate+minerals+ribose+synthesis&cd=1&hl=en&ct=clnk&gl=us
And on the phosphorylation issue we discussed earlier, chemical phosphorylation is possible without enymes. Granted, if we are talking about pre-enzymatic organisms we are not talking about LUCA, but rather some ancestral, possibly precellular organism. But the point stands that the evolution of nucleotides can occur through a chemical process outside the control of the RNA or DNA bases its acting on. This link below describes an experiment that references and builds on the Shapiro formaldehyde study in your Harvard abstract:
http://www.jbc.org/cgi/content/full/282/23/16729
So in that primordial soup can not only contain phosphates, it can also contain natural catalysts to drive the phosphorylation of the nucleosides generated in the Miller Urey experiment into the nucleotides needed for life. With this we have all the ingredients for the first RNA (pre-LUCA), and using existing external chemical sources of energy, we also have everything we need for RNA or DNA replication, using the model I described a few days ago where the denatured strands of base pairs serve as templates for replication without enzymes.
The problem at this point becomes how the system of repair and replication was internalized into the cell, even when the cell first appeared (some suggest that it came rather late, see http://en.wikipedia.org/wiki/Iron-sulfur_world_theory ). We still don’t know step by step the exact path evolution took, but it is an area of active research and what we do know for certain is that the environment of the ancient Earth had everything it needed to cross the boundary between chemistry and biology. We know that the first organisms had to and could depend on that environment to provide them with the energy and the building blocks it needed to begin evolving into something new.
Tom, PCR and more phosphorylation
So in one of your latest posts you discussed the mechanism of PCR. Here’s the thing. For my purposes it’s largely irrelevant since we can bypass it entirely and form the phosphodiester bond without it (I cite that claim below). The idea is that since we are dealing with evolution, we cannot begin with the assumption that a specific mechanism sprang into existence fully formed. What we know is that we have a need for some general functionality. What that functionality is will depend on what organism we are dealing with. Pre-LUCA, we are somewhere in between chemistry and biology, so some of the tasks that modern organisms handle with their modern mechanisms must be somehow shared or divided between some simplified, rudimentary mechanism of the organism and the basic chemistry of its environment. That’s what we know is possible with some of the studies I’m citing in these posts. So you said this earlier:
[quote]If we extrapolate this fact to early form DNA, you find that you have to be able to channel a lot of energy from somewhere into the phosphodiester bonds that are the links in the DNA chain. Modern cells use mostly glucose metabolism to create the ATP, CTP, GTP and TTP necessary to replicate DNA AND they have to use enzymes that link them on the 3 and 5 locations of the 5-member deoxyribose sugar. if they link to say, the 2 location instead of the 3, then no DNA as we need it. Linking in somewhat random locations would be what happened if chemical reactions without enzymes were the basis of these reactions.[/quote]
And that’s fine. It doesn’t need to work every time to be a good enough starting point. So (cited below) we have a feasible solution that relies entirely on the environment for nucleotide synthesis by chemical phosphorylation. And it is inefficient, as you noted. The Costanzo experiment (Nucleoside Phosphorylation by Phosphate Minerals http://www.jbc.org/cgi/content/full/282/23/16729 ) readily acknowledges that 3 or 4 species of linked nucleotides occur, including 3’:5’ and 2’:3’. Interestingly, under the discussion they note that the stablest 2’:3’ species may also have been of some use:
[quote] It was actually shown … that 3′,5′-linked hexa-adenylic acid with a 2′:3′-cyclic phosphate terminus couples on a polyuridylic acid template in the presence of ethylene diamine to form the dodecamer and octadecamer. The bond produced was largely that of the 2′,5′-isomer, but 5% of 3′,5′-bonds also formed.[/quote]
This shows that the primordial environment can handle phosphorylation well before the evolution of polymerase chain reaction. The question of how a self contained unit of RNA first began to self-polymerize is also being researched with promising results. There are several studies, including one in which RNA which can self-catalyse its own replication, for example. We have some evidence of that as well in a lab-created RNA strand (http://www.sciencemag.org/cgi/content/abstract/292/5520/1319 ).
We also have RNA strands that can act initiate duplication by facilitating the copying of secondary RNA strands in the absence of enzymes and proteins (http://www.cell.com/chemistry-biology/abstract/S1074-5521(98)90294-0 )
And finally, this one describes an observed mechanism to handle nucleotide synthesis using RNA alone, thereby negating any need for PCR (http://www.nature.com/nature/journal/v395/n6699/full/395260a0.html )
So we have the functionality of replication and phosphorylation, even if only crudely, without the complex and efficient modern mechanism. So to quote you again:
[quote]There is one more problem with using systems like PCR as an example of how early DNA could be copied. PCR has a designed component to it which is not allowed according to the rules of evolution. PCR does not work without the use of a primer strand.[/quote]
The idea is that if we are talking about the early evolution of of DNA/RNA replication, we are not talking about PCR yet. The system, actually NO system, began fully formed. That’s the sticky part, and in a nutshell the difference between evolution and creation. What we ultimately find is that there are other solutions in the absence of sophisticated metabolic tools that are simple and imperfect but which can do the job. That’s all the slack we need to evolve the more efficient models.
The ability to rely on these simpler systems for energy and replication allows the organism time to begin the development of control mechanisms like PCR, and allows evolution plenty of time to tinker with its “design” so that a few billion years later, you may well end up with a system so well honed that it seems too perfect to have had humble beginnings. But that’s because evolution is awesome =).
The discussion seems relevant to Slugsie’s question because the difference in Microevolution and Macroevolution is the difference in origin. The Microevolution perspective starts with design and whatever evolutionary processes happen do so as a result of a designed capacity to change. The Macroevolutionary perspective is that we started without design and that non-directed processes brought about life as we know it and all it’s capacity for evolutionary change.
I have been arguing that Macroevolution cannot be true because the fundamental DNA, RNA, protein and cellular biology have co-dependant factors like DNA cannot be copied without an enzyme that itself has to be coded in the DNA. DNA without replicating enzymes is worthless. Replicating enzymes cannot exist without DNA. They are both necessary for DNA replication but neither is sufficient.
This co-dependence problem plays out all over the place in the molecular biology world. You can’t have a viable cell without both metabolism AND genetic inheritance. Each one is necessary but neither is suffucient. When you have simultaneous co-dependence like this, it points to design. Even if the scale is only slightly tilted toward design for one occurrence of simultaneous co-dependence, the number of co-dependent factors in life is very large so the large number of them in total points heavily toward design. Take meiosis as another example. Which came first, the sexual reproduction that re-unite gametes or the meiotic division that made the gametes? Both are necessary for sexual reproduction but neither is sufficient.
What I have been trying to pin-down with all this discussion regarding pre-LUCA evolution is that evolutionary processes that are present today cannot be the same processes that get us from one cell to the modern biota. Here is the key point: in early evolution DNA has to start short and get longer to allow for increased complexity. When we take a look at all the hereditary insertion mechanisms that are available, they are functions of transposons, retroviral action, errors in meiosis, and human genetic engineering. All of these (except for human engineering) require advanced protein/enzyme complexes that would have to have evolved WITHOUT the benefit of insertion mutations. Thus, you have to elongate the DNA in early evolution but cannot do it because all the elongation mechanism are only present in the modern biota. This is the basis of my claim that modern life has to be designed.
I will research the RNA world hypothesis more fully, but one of the truths to the RNA world hypothesis is that neither circular DNA nor straight DNA could have been the first genetic information because both models are critically flawed. Even if RNA world is true, it has to be gone by the time LUCA is on the scene because the transcription and translation mechanisms are part of the LUCA definition. Since meiosis is NOT part of LUCA, most of the basis for insertion mutations are not present either. Thus, even if RNA world is true, you can’t get from LUCA to meiotic cells because you don’t have adequate insertion mutation capability.
Think I addressed some of these concerns in my latest posts, will be back as soon as I have time for the circular RNA/DNA discussion.
Autumn, let us look at these one at at time. regarding your claim to environment-based phosphorylation:
[quote] The Costanzo experiment (Nucleoside Phosphorylation by Phosphate Minerals http://www.jbc.org/cgi/content/full/282/23/16729 ) readily acknowledges that 3 or 4 species of linked nucleotides occur, including 3’:5’ and 2’:3’. Interestingly, under the discussion they note that the stablest 2’:3’ species may also have been of some use: [/quote]
Scope of the experiment
This experiment starts with already created nucleosides, medium-high temps (90C to 250C in places), pulverized solid phosphate crystals, essentially pure formamine, and a required absense of water. It produces mono nucleotides (not activated). It does not produce any phosphodiester bonds. It does not create DNA or RNA in any form.
Issues:
1. This experiment claims to be pre-biotic. Why? Because the article clearly states that this method doesn’t work in water. In order to form a cell membrane you have to have water inside and outside the cell. The membrane interaction with water is how the membrane works.
quote from article:
Thus, activated nucleic monomers can form in a liquid non-aqueous environment … providing a solution to the standard-state Gibbs free energy change problem.
2. The article describes the fact that polynucleotides (DNA and RNA), polysaccharides, and peptides (proteins) cannot form in aqueous environments due to free-energy limitations.
quote from article:
Polymers (polysaccharides, peptides, and polynucleotides) will not spontaneously form in an aqueous solution from their monomers because of the standard-state Gibbs free-energy change.
3. The article states a limiting fact about the origin of life due to chemical requirements.
quote from article:
either (i) life did not arise in aqueous environments, or (ii) pre-genetic polymerizations required activated monomers.
4. You mis-represented the quote from the paper as saying that a poly-nucleotide chain (RNA in this case) can be formed without existing RNA. The passage says that a short poly-A section formed complementary to an already present poly-U template. Thus you had to have poly-U RNA before the environment would make small poly-A sequences based on Poly-U. Furthermore, this reaction has to be done without water present or else no polynucleotide (phosphodiester) bonds will form. This is a fundamental problem because you have to be able to elongate the RNA/DNA in a water environment once the first cell forms. The article and your statement are re-quoted below.
[article quote] It was actually shown … that 3′,5′-linked hexa-adenylic acid with a 2′:3′-cyclic phosphate terminus couples on a polyuridylic acid template in the presence of ethylene diamine to form the dodecamer and octadecamer. The bond produced was largely that of the 2′,5′-isomer, but 5% of 3′,5′-bonds also formed.[/article quote]
[your quote]the primordial environment can handle phosphorylation well before the evolution of polymerase chain reaction[/your quote]
Summary:
This article brings the Gibbs free energy problem associated with DNA and RNA elongation into this discussion. It is a fact that DNA, RNA, nucleotides (such as AMP, ADP and ATP)proteins and sugars will not form in cellular aqueous environments without something analous to enzymes to transfer free energy from one chemical bond to another.
Even IF you can form these precursor chemicals in a highly-reducing non-aqueous environment, it only serves to increase the difficulty of the simultaneous coincident that what created these chemicals is not able to be used once a membrane wraps them up and they are now inside an acqueous cell.
Tom, the Costanzo experiment:
[QUOTE]Scope of the experiment
This experiment starts with already created nucleosides, medium-high temps (90C to 250C in places), pulverized solid phosphate crystals, essentially pure formamine, and a required absense of water. It produces mono nucleotides (not activated). It does not produce any phosphodiester bonds. It does not create DNA or RNA in any form.[/quote]
Yes, yes, and yes. But I think you missed the point. This was not in reference to the creation of nucleosides (we covered that earlier) or of RNA or DNA, but to the phosphorylation of nucleosides to nucleotides, which you previously claimed was not possible. What I said was:
…we have a feasible solution that relies entirely on the environment for nucleotide synthesis by chemical phosphorylation…
to refute the point you made earlier about not having free nucleotides in the primordial soup. We can create them abiotically, period.
[quote]4. You mis-represented the quote from the paper as saying that a poly-nucleotide chain (RNA in this case) can be formed without existing RNA.[/quote]
No, I never attibuted that claim to this study, but you are correct that I assume it. What I said about this study was that it’s been proven possible to use RNA to facilitate the copying of another RNA strand, or as a catalyst for replicating itself. My claim is that this is possible without PCR, which you insist must catalyze these reactions, and the studies I cited establish that.
You said:
[quote]3. The article states a limiting fact about the origin of life due to chemical requirements.
quote from article:
either (i) life did not arise in aqueous environments, or (ii) pre-genetic polymerizations required activated monomers.[/quote]
Yeah, I saw that. Their solution to this is an hypothesis. Long quote ahead:
[quote]Our working hypothesis is that water combined with HCN, affording formamide, thus quenching its reactivity and instability. Based on its wide liquid range (4–210 °C) and limited azeotropic effects, formamide could have easily formed highly concentrated or completely anhydrous solutions.
…
At temperatures higher than 100 °C, the presence of water would not have posed a long-lasting stability problem.
By simple heating in the presence of common catalysts, formamide yields a complete set of nucleic bases (48–51), acyclonucleosides (52), creates conditions in which phosphoester bonds in polymers are more stable than in the monomers (14, 53), and favors the formation of micelles (54, 55). The novel property of formamide described here, efficient phosphorylation of nucleosides from minerals, provides one more missing link in the identification of a single unifying chemical frame for the self-organization of nucleic polymers in prebiotic conditions.[/quote]
So the idea is that we are still in solution, but with extremely concentrated formamide rather than water. Fortunately for evolution, this may not be the problem you think it is. Nucleotides, once phosphorylated, are quite stable in water. It’s ONLY the phosphorylation step that requires the formamide (or whatever they decide is the effective dehydrating solution).
So the question of how to get the nucleotides into the cell or to polymerize is not one of getting it there without letting it touch water, its the same question we’ve had all along. How do we get from free nucleotides and RNA/DNA to a celled RNA and DNA? I’ll be back to you on that one.
[quote]
This article brings the Gibbs free energy problem associated with DNA and RNA elongation into this discussion. It is a fact that DNA, RNA, nucleotides (such as AMP, ADP and ATP)proteins and sugars will not form in cellular aqueous environments without something analous to enzymes to transfer free energy from one chemical bond to another.[/quote]
OK, I pointed out in my Aug 12 post (photosynthesis and glucose), we DO get sugars in Miller-Urey, which is in a heated aqueous solution and is a chemical process without the use of enzymes.
In my Aug 21st post (phosphorylation), I show we can also get the sugar ribose, which you earlier contested. This is also an aqueous, chemical process.
In the recent posts referencing the Costanzo experiment, I show that we get nucleotides (non-aqueous, true, but the nucleotide byproducts are fine in water). Chemical process.
What I have NOT shown is the step from nucleotides to RNA. Would be really cool if I had. There’s some work in that area, but from what I’m reading its still up in the air. I’ve not heard of anybody building RNA from scratch in a lab as of yet. It would be plastered all over teh news if they had, “Scientist Creates Life in a Petri Dish”.
TOM,
OK, I just caught on to what you were saying about the PCR. I’ve been confusing my terms. I was writing PCR and thinking about kinases, so now what you said about the studies not relating to PCR makes sense. Sorry about that.
So you are right. They, or at least those related to phosphorylation, do not circumvent PCR, they are phosphorylating the nucleosides and circumventing any need for kinase (and whatever other enzymes handle phosphorylation) activity. The PCR bit, linking the nucleotides, was done in another study I mentioned using just an RNA strand, but that still leaves me with the question of how the first RNA formed that could self-replicate.
I have been reading for quite some time and trying to follow everyone’s posts…quite in depth I might add….and have come to one conclusion. Tom…whoever this guy is…certainly has made great arguments concerning evolution or lack there of; Autumnn, no matter how bad you want to negate everything Tom is saying, you are not acheiving that status, not even coming close. It seems that Tom carried his points across well enough to keep you continually on the defensive and you never could take a good foot hold to assume the offensive, which in my eyes points me to think you are either weak minded or your argument is horribly flawed. I will choose the latter as the first must be negated in regards to previous posts.
Interestingly enough, my understanding is that Micro-evolution is actually de-evolution. From what I’ve read here, in these posts alone, when “Christians” claim “micro” they are only claiming that out of ignorance and not out of factual info.
I have to completely disagree with you. Evolution is a fact (and a theory), so that leads me to conclude that Toms arguments have a fundamental flaw. No idea what it is as I’m no biologist.
I’ll also state once again, it’s only Christians that claim a difference between Macro- and Micro- evolution. To biologists there is no difference. Any change of the genetic makeup of a population is evolution.
Sorry you feel that way Allen, naturally I disagree. Tom is an old school friend of mine and I respect his opinions, but we clearly don’t see eye to eye on this one.
As for being on the defensive, of course I am. I have no interest in attacking or challenging (for the purposes of this discussion) the merits or lack thereof of creationism or intelligent design. My purpose here is to *defend* the established facts of evolution which Tom is challenging. That should have been obvious.
You make some strong criticisms, but you neglect to indicate exactly what you feel is the problem with my logic. If you’d like to point out which of my arguments is “horribly flawed”, feel free. I’m sure I can make time for you.