Darwin re-visited

[Biochemist]

Do you have any thoughts as to how speciation might be "pre-coded" in the genome?

Not really. This is the abiogenesis discussion. Abiogenesis has always been pretty poorly described, other than through thoughtful conjecture. The old Oparin experiments where he ran electricity through a methane/carbon atmosphere and got some trace nucleic acids (or precursors-I forgot) led many to sort of assume that the first life architecture arose out of this sort of hostile environment.

 

There are a lot of difficulties with this argument. Notably, that even the 'simplest' life forms (bacteria?) are reasonably sophisticated little machines. If fthe first life form arose 3.5 billion years ago, and we allow for some time to let the earth cool (500 million years?- help me on this), this allows for 500 million years to create, in a truly random fashion, the single successful life architecture (DNA, RNA, 20 amino acids, and replication therein). Seems like a tall order.

 

My hypothesis puts even more complexity onto the first life form, but it is probably only a several orders of magnitude greater than it was already.

 

I suspect the folks that are interventionists (i.e. "aliens did it") would like my hypothesis.

[Biochemist]

You are continually arguing against a "natural" expanation for speciation, for instance, yet deny supporting a "supernatural" one.

By the way, I think this is all natural. I am a theist, but (speaking as a theist) God usually works through established processes. Science has undeniably established that.

 

It is not reasonable, even as a theist, to expect that God did some "magic pzapffft" (do try to pronounce that) and life showed. Maybe the big bang counts as the one "magic pzapffft". The one trend in science (really, in all branches) is that, the more we learn, the state of nature gets more complex than we ever anticipated.

 

Makes life fun.

[modest]

We do have dozens of examples of selection (as Modest offered above) where environmental changes result in selection of a normal variant.

Huh?

 

I think speciation is pre-coded in the genome of the parent species.

 

Easily confirmed, is the genome for a human or a lizard or a chicken to be found in a bacterium?

 

~modest

[Turtle]

Not really. This is the abiogenesis discussion. Abiogenesis has always been pretty poorly described, other than through thoughtful conjecture. The old Oparin experiments where he ran electricity through a methane/carbon atmosphere and got some trace nucleic acids (or precursors-I forgot) led many to sort of assume that the first life architecture arose out of this sort of hostile environment. ...

 

You could at least hunt up some details on that electrical business, so we can see what your reasons are for dismissing it out of hand. :eek: Then too, as you say it is 'old', so maybe you missed something new while you were kicking that horse? :hyper:

 

Harvard Gazette: A role for clay in formation of the first cells

Harvard News Office

 

Harvard researchers demonstrated how the first living cells may have formed in a series of experiments that indicate that clay can be an important catalyst for life.

 

While the research is a far cry from proving that humans sprang from clay, as some creation myths assert, it does provide a possible mechanism for explaining how life initially arose from nonliving molecules.

 

Researchers at the Howard Hughes Medical Institute and Massachusetts General Hospital showed that the presence of clay aids naturally occurring reactions that result in the formation of fatty sacks called vesicles, similar to what scientists expect the first living cells to have looked like.

 

Further, the clay helps RNA form. The RNA can stick to the clay and move with it into the vesicles. This provides a method for RNA's critical genetic information to move inside a primitive cell. ...

 

On the whole I find any of these theistic arguments disengenuous in forwarding science. Perhaps I wouldn't take such offense if there was afoot a concerted effort among scientists to join theistic forums and attack their doctrines etcetera, but that is not the case as far as I have seen.

 

Fianlly, any of these anti-science/theistic arguments about the unlikely chance -probability- of this or that occuring have no scientific or mathematical merit.:) Stuff happens. :doh:

 

I now return you to our regularly scheduled Darwin experts.....................

[Biochemist]

Easily confirmed, is the genome for a human or a lizard or a chicken to be found in a bacterium?

Of course not. The complexity is that DNA modifies DNA. We have probably a half dozen DNA modification mechanisms (e.g., transposons, chromosome crossover, etc) that change DNA sequence. I am sure we will find more. We could posit that these are "random", although most of these alterations follow a narrow set of possibilities.

 

It would be as easy to posit that at least some of these are so likely as to be construed as "coding". This is not DNA coding for mRNA (and hence proteins), it is DNA coding for a DNA change. This would (of course) mean that the genes would change throughout the tree of common descent. It also might suggest that higher organisms would accrue increasing quantities of non-transcribing DNA since the sophistication of the DNA self-coding would logically increase in complexity over time, hence the volume of non-transribing DNA would increase to handle the increasing complexity.

 

Perhaps most tellingly, the "code" would have an "end". That is, it would get to the end of the program. You could argue that when we got to the 70 (or so) phyla at the end of the Cambrian, that was the "end" of the program. We have lost 30 or 40 phyla since then, and there is no evidence of a new one popping up.

[Biochemist]

You also seemed to miss the part about genetic analysis in the paper about the lizard population:

Gala- I really appreciate you giving this thread this quality of attention. I think either I missed your point, or you missed mine. My point was simply that rapid adaptation is generally at odds with mutative causality. Your point that the two lizards are genetically identical (which is, I think, what you underlined above) demonstrates conclusively that both the original and the adapted form were the same genotype. Ergo, this adaptation was not driven by a mutation. Rather, this particular adaptation is a feature of this particular genome. The same genome can produce either morphology.

 

Am I missing your point?

 

Bio

[modest]

Easily confirmed, is the genome for a human or a lizard or a chicken to be found in a bacterium?

Of course not.

 

So, speciation is not pre-coded in the genome of the parent species.

 

If prokaryotes living before the Cambrian explosion had in them the blueprints to make complex multicellular organisms, then they still would have that blueprint either in the form of DNA or RNA or some other mechanism. Nothing like that has ever been found.

 

An E. coli cell simply does not have an intelligence or "program" inside it to make complex life forms. You are describing something that simply isn't there.

 

~modest

[Galapagos]

I think speciation is pre-coded in the genome of the parent species. It fits the available facts better.

How would the information get "pre-coded" into the genome?

According to modern biological science, natural selection is basically coding information about the environment into genes so it can be used by the offspring of the next generation.

What mechanism could know in advance what immediate challenges a given population would face?

 

It explains the following, each of which are at odds with speciation-by-mutation:

You are going to need to clarify this. How are these at odds with current evolutionary thought? Please be specific.

 

1) the apparent expression of recessive alleles that were not previously expressed

2) the speed of speciation

3) the particular issue of increased speciation with sequestered populations- recessive alleles express even when there was not necessarily adequate time to create them- and LOTs of them (addresses the mechanism of the Cambrian explosion)

4) the common biochemical roots of all life forms (e.g., DNA, RNA, the same 20 amino acids- a very troublesome problem)

5) The tendency of higher forms to have more "junk" DNA than lower forms (since non-coding DNA would be required to manage evolution of DNA, and more would be required in higher forms)

6) the fact that phylogenesis seemed to have stopped a couple hundred million year ago

 

It certainly does not address the abiogenesis problem. But we had that problem anyway. We just made that problem bigger.

 

I do not know anything about number one in your list.

I think that 2, 3(not sure about this "not enough time/recessive" stuff though), and 6 are very well covered in the current literature. There are many possible causes for the "cambrian explosion"(see various explanations here and here). I also think the theories of punctuated equilibrium and allopatric speciation explain much about tempo of speciation.

Number 4 is best explained by common descent. We share chemistry because we are all related.

As for number 5, I would refer you to the onion test:

Junk DNA and the Onion Test

The onion test is a simple reality check for anyone who thinks they have come up with a universal function for non-coding DNA. Whatever your proposed function, ask yourself this question: Can I explain why an onion needs about five times more non-coding DNA for this function than a human?

Please read the whole article linked above. It was written by evolutionary biologist T R Gregory, who specializes in genome size evolution.

 

Also regarding 6, your use of "higher" and "lower" implies progress in evolution(according to the modern synthesis, organisms adapt to local, immediate pressures). I feel like the same notions of teleology are present in your claim about "pre-coding" in the genome; selection maintains and changes the code according to modern biology-- how is it coded beforehand in your explanation?

I would also direct you to the page on C-value paradox before you want to comment on Junk DNA again:

The C-value enigma or C-value paradox is a term used to describe the complex puzzle surrounding the extensive variation in nuclear genome size among eukaryotic species. At the center of the C-value enigma is the observation that genome size does not correlate with organismal complexity; for example, some single-celled protists have genomes much larger than that of humans.

C-value enigma - Wikipedia, the free encyclopedia

[Galapagos]

Gala- I really appreciate you giving this thread this quality of attention. I think either I missed your point, or you missed mine...

 

Bio

 

That was a misunderstanding and hasty response on my part. Sorry about that.

 

Regarding morphological changes and alteration of DNA... not all inheritance is genetic.

Here is a good summary by evolutionary developmental biologist PZ Myers of what is known as epigentic inheritance. This would include factors such as histone modifcation and chromosomal arrangement. The point is that not all change needs to depend on base-pair changes.

 

Another idea that is currently being debated by biologists would be the role of cis regulatory elements in evolution. Scientists like evolutionary developmental biologist Sean B. Carroll have recently claimed that morphological change is due to alterations in what are known as cis regulatory elements, and then scientists like population geneticist Jerry Coyne have criticized his work as being presumptuous.

 

Here is an article by Carroll in Scientific American about his ideas, I quote his key points:

Regulating Evolution: How Gene Switches Make Life: Scientific American

-Because genes encode instructions for building animal bodies, biologists once expected to find significant genetic differences among animals, reflecing their great diversity of forms. Instead very dissimilar animals have turned out to have very similar genes.

-Mutations in DNA “switches” that control body-shaping genes, rather than in the genes themselves, have been a significant source of evolving differences among animals.

-If humans want to understand what distinguishes animals, including ourselves, from one another, we have to look beyond genes.

More about this debate can be read here:

evolgen archive: The Genotype and the Phenotype and How to Measure Divergence

evolgen archive: Coyne versus Carroll

Also, here:

Hurrah! Yet another controversy in evolutionary biology!

 

There is also a good video lecture of Coyne stating his case regarding Carroll on youtube for anyone interested:

YouTube - Year of Darwin - The Locus of Evolution http://www.youtube.com/watch?v=JraAzQs15zM

 

I'm on the sidelines for this sort of debate(cis reg elements, not this thread), as I am but a humble student. I am also not at all swayed by the misrepresentation of the state of the art by both Hbond and Biochemist so far in this thread. At the very least, the two of you need to hit the books(or online articles, or whatever) before you try to submit your armchair speculation about evolutionary biology if you want to be taken seriously.

[REASON]

So, speciation is not pre-coded in the genome of the parent species.

 

If prokaryotes living before the Cambrian explosion had in them the blueprints to make complex multicellular organisms, then they still would have that blueprint either in the form of DNA or RNA or some other mechanism. Nothing like that has ever been found.

 

An E. coli cell simply does not have an intelligence or "program" inside it to make complex life forms. You are describing something that simply isn't there.

 

~modest

 

I think that's a good point, modest.

 

As a follow up I would suggest that the fact that the evidence shows that prokaryotes have evolved into more complex species only reveals the potential of DNA. What's missing is an external force or mechanism to trigger the evolutionary process.

 

No matter what the perceived odds, the fact is it has happened. Speciation has occurred. I think Bio would agree with that. But only a natural explanation can be revealed through science.

[Biochemist]

So, speciation is not pre-coded in the genome of the parent species....An E. coli cell simply does not have an intelligence or "program" inside it to make complex life forms. You are describing something that simply isn't there.

I don't think you picked up my point. The genes of higher species are certainly not in lower genomes. But my suggestion is that the genomes have predispositions for DNA alterations.

 

Your assertion that E Coli does not have a program (other than for protein coding) in its DNA "because we have not found it" is as speculative as my assertion that it does have one.

 

Bio

[Biochemist]

As a follow up I would suggest that the fact that the evidence shows that prokaryotes have evolved into more complex species only reveals the potential of DNA. What's missing is an external force or mechanism to trigger the evolutionary process.

DNA certainly is high in potential. This alone is one of the dilemmas. The VERY first life form uses the very same DNA and the VERY same 20 amino acids as all current life forms (with very rare exceptions on some amino acids that are modified after DNA coding).

 

We also know something about "external forces", in that the fossil record suggests that we get increases in speciation whenever an environmental cataclysm sequesters a large population into small groups. This is the outcome we would expect when recessive alleles are extant in a population. They are more likely to be expressed when the population is small. It does NOT explain how the recessive alleles got there, if they were never previously expressed.

 

Bio

[Biochemist]

Regarding morphological changes and alteration of DNA... not all inheritance is genetic.

If by "genetic" you mean contained within genes, agreed (and reasonably well established). But inheritance (by definition) is genomic, which includes the entire body of DNA (the vast majority in humans) that is not genes.

The point is that not all change needs to depend on base-pair changes....Another idea that is currently being debated by biologists would be the role of cis regulatory elements in evolution. ...At the very least, the two of you need to hit the books(or online articles, or whatever) before you try to submit your armchair speculation about evolutionary biology if you want to be taken seriously.

Gracious. This is a site that is heavily leavened with armchair speculation.

 

Gala, I really appreciated that link on the "new" controversy, discussing the battle over the importance of cis regulation. We have really only scratched the bare surface on the importance of the non-protein coding DNA. In humans, it is 98% of the genome. We do know about dozens of actions of this code, but most we have little or no idea.

 

The author in your link brings up the sociological question of why scientists get into such conflicts over contrasting ideas. Probably a good topic for another thread.

[Biochemist]

How would the information get "pre-coded" into the genome?

That would be an abiogenesis discussion. Should be the topic for another thread. Yes, I am dodging the topic. All views of abiogenesis are so poorly supported (in my view) that they are all equally weak.

According to modern biological science, natural selection is basically coding information about the environment into genes so it can be used by the offspring of the next generation.

Sort of. The current view of natural selection is that rare variants in the population are advantaged in particular niches, hence those variants are favored. Natural selection per se really only applies after the point where a genomic changed can express itself in the population (and hence have the potential for selection). What we are discussing how the genomic change got into the population.

You are going to need to clarify this. How are these at odds with current evolutionary thought? Please be specific.

 

Let me give it a shot, one-by-one:

1) the apparent expression of recessive alleles that were not previously expressed

The fossil record still reflects the uneven rate of development of phyla as first described by Gould and Eldredge in 1972, and generally referred to as Punctuated Equilibrium. To the extent that we can explain PE, it is a logical consequence of sequestering small populations from large ones. Small populations are more likely to express recessive alleles (arithmetically). Ergo, any cataclysm that eradicates a large fraction of a population, or sequesters portions of a large population should result in increased expression of recessive alleles. The fossil record supports this. It does NOT explain how the recessive alleles got there. To the extent that we get large numbers of recessive alleles expressed suddenly, it is not particularly consistent with a mutation-selection-mutation-selection sequence, since the time required would be egregious.

2) the speed of speciation

This is the Cambrian Explosion problem. Many have rationalized the Cambrian Explosion (the advent of about 70 phyla over perhaps 300 million years) as an artifact of the fossil record (possible) or that the mutative processes are so constrained that any probabilistic assessment of mutative success grossly underestimates the probability of success (also possible). But the plain interpretation of the fossil record is that we were reasonably dormant (in terms of creation of new phyla) until about 500 million years ago (maybe three existed), then we "suddenly" got 60+ new ones over 300 million years, then we stopped and lost 30 or 40 (depending how you count) over the next 200. This path does NOT look like serial mutation. This rapid acceleration in genesis of phyla, followed by cessation of new phyla creation is grossly at odds with a serial mutation mechanism.

3) the particular issue of increased speciation with sequestered populations- recessive alleles express even when there was not necessarily adequate time to create them- and LOTs of them (addresses the mechanism of the Cambrian explosion)

I think I discussed this above.

4) the common biochemical roots of all life forms (e.g., DNA, RNA, the same 20 amino acids- a very troublesome problem)

This is a particularly odd one, and rarely discussed, since it is really more related to abiogenesis than speciation, but it relates to our current discussion. All life forms use exactly the same life architecture (DNA, RNA, and 20 amino acids). Why is there no other life architecture? Why are there no DNA variations? Why, for goodness sake, are there NO other amino acids used (out of the infinite array of possibilities) than the standard 20? Is it reasonable to suggest that the VERY FIRST life form (presumably some prokaryote) would be able to incorporate 20 amino acids for its parochial purposes, and then we find out 3.5 billion years later that the exact same elements can build MUCH more complex life forms? You could certainly assert that once the "life" ball started rolling, the existing life forms were the only ones replicating, and hence their proteins (which were replicating) became the most available substrates. Reasonable enough. But never a new amino acid in 3.5 billion years? Shouldn't there have been thousands of other amino acid choices in the primordial sea that were potential substrates in the early millenia? Should make you go "Hmmm".

5) The tendency of higher forms to have more "junk" DNA than lower forms (since non-coding DNA would be required to manage evolution of DNA, and more would be required in higher forms)

This is probably my weakest argument, but the fact that the non-protein-coding DNA increases as we climb the evolutionary tree is interesting. The cell is remarkably efficient at eradicating any spare parts, certainly proteins. The lysosomal system effectively removes any ubiquitin-tagged protein and "takes out the trash". The ubiquitin tagging process is a little mystic (i.e., why do these proteins get tagged?), but the efficacy is undeniable. Now, if we hypothesize that the nucleus is as grossly inefficient at clearing out bogus DNA as the cytoplasm is efficient at clearing bogus protein, we are OK. But the more we learn about non-protein-coding DNA, the more important it gets. Your references above include some of the discussion about higher phyla morphology being dependent on non-gene-coding DNA (such as cis and trans regulatory code). Ergo, the more complex the phylum morphology, the more requirement for non-gene DNA. This code barely exists in lower life forms (I think bacteria are 98%+ genes- someone help me here). Humans are under 2% genes. So we are suggesting that this single DNA/RNA/20 amino acid architecture (descirbed above) not only launched the first life form 3.5 billion years ago, but also provided a mechanism for a completely different coding structure that was not even necessary for another 2 billion years? Should make you go "Hmmmm" again.

6) the fact that phylogenesis seemed to have stopped a couple hundred million year ago

Following the weak argument above, we have the strongest one. It appears that we had 70 phyla at the end of the Cambrian explosion, and we have subsequently lost 40 (both numbers rough). This is completely at odds with speciation-by-mutation. This is typically rationalized by saying that the "niches are all full". Really? What it really looks like is that phylogenesis ran for 3 billion years and stopped. My suggestion is that it stopped because the "program" ran out.

I think that 2, 3(not sure about this "not enough time/recessive" stuff though), and 6 are very well covered in the current literature. There are many possible causes for the "cambrian explosion"(see various explanations here and here). I also think the theories of punctuated equilibrium and allopatric speciation explain much about tempo of speciation.

As I mentioned above PE better supports my position that speciation-by-mutation. And I described allopatric speciation above without naming it.

Number 4 is best explained by common descent. We share chemistry because we are all related.

I accept common descent. That is the problem, not the solution. The question is why there is exactly one life architecture? Not two?

Also regarding 6, your use of "higher" and "lower" implies progress in evolution(according to the modern synthesis, organisms adapt to local, immediate pressures).

I really just used higher and lower to refere to later (in the tree) versus earlier

I feel like the same notions of teleology are present in your claim about "pre-coding" in the genome; selection maintains and changes the code according to modern biology-- how is it coded beforehand in your explanation?

Again, I have no position on abiogenesis. But think that abiogenesis is so poorly circumscribed, that we should look at the data and se where it points us.

 

This is a little similar to the big bang theory. No one really asks the question about how that first singularity got there. But the astronomical evidence points to it (along with a bunch of really ugly math) so we sort of assume that the universe started in a "point" even though it is pretty counterintuitive. I think about abiogenesis the same way. The fact that I inserted more information load into the first life form does not really bother me. It is just something else to figure out.

[HydrogenBond]

The point I was making is genetics sets the potential but before this can be utilized for selective advantage other things need to occur. Let me go through a thought process. Say we have a random change on the DNA that produces a useful gene. It all depends on where that change occurs. If it occurs in areas of the DNA that are not normally active it is a diamond in the rough that may just sit there among what is called junk genes (in the attic). Over time it can be randomly changed again and the potential is lost.

 

This same gene will have a better chance of integration if it occurs in a more active area of the DNA. But here, even random has problems. If random changes the start and stop sequence it may never get started or it can end up much to long as transcription goes past what should be a stop.

 

Let us make it easier and limit the change to inside an active genetic area within an existing start and stop. Making mRNA and translating protein uses a basic schema so we can make this protein. The next question is where to put it? If it is close to the original, we put it where the original goes. Say it was 50% faster at a given task. If it was part of an enzyme train, it can still only produce as fast as the weakest link in terms of output production. It has the potential to go faster at position 3, but position 2 is still slow and can't feed it input fast enough to use its full capability. There is no major advantage until be also change #2.

 

Say we are fortunate and it happens to fall into position 1. It can crank out product, for enzyme 2, but 2 is still slower. This may waste energy and have an impact as product begins to backlog and needs to be recycled. The cell was better without the upgrade since now fuel costs have gotten higher for the same.

 

Let us get more complicated than an easy replacement within the cell. If we place it where the former went, but now it doesn't do this task, we will mess up the entire enzyme train. Do we flood the cell with this new enzyme, blindly hope it finds a good spot? That could mess up other areas too. There are thousands of places to put it, with only one sweet spot. We need a plan that can do this time and time again or else every genetic change will be an accident waiting to happen, since there are more things that can go wrong.

 

Transport into the cell is often very specific. Our new enzyme finally gets its place and can crank out B. But we don't have a shipping and receiving enzyme yet to bring in the product and convey it to the enzyme. Will the cell let it sit idle while we wait for the DNA to randomly make the correct one or will it recycle it? Even when we get a transport protein, where do we put it. So we place it, is the other enzyme still there? Even if it is there, why is it way over there, that seems like a waste of energy. How do we get the cell to bring it closer?

 

The DNA has the easy job with only 4 things to worry about and its gold coming from mistakes. The rest of the cell has to make it work. The current model is oversimplified. I am not saying genetics is not at the inception of the process and selective advantage is the result, but there is also a middle zone which interfaces these two bookends.

[Biochemist]

The point I was making is genetics sets the potential but before this can be utilized for selective advantage other things need to occur.....The DNA has the easy job with only 4 things to worry about and its gold coming from mistakes. The rest of the cell has to make it work. The current model is oversimplified....

Thanks HB. You did a nice job of offering another example of the complexity (analogous to my verbose entry in post 463 about a new enzyme system). If we assume that all of the processes and services that you describe are also coded by DNA, then the raw quantity of synergistic DNA changes required for a positive funcitonal change seem pretty challenging to implement. This is why I think a mutative mechanism as a primary driver for speciation is so unlikely.

[modest]

I think speciation is pre-coded in the genome of the parent species.

 

The genes of higher species are certainly not in lower genomes.

 

Clearly someone is confused.

 

~modest