Darwin re-visited

[Moontanman]

This is a really interesting theoretical point, FT. The notion that the first life form rapidly migrated to multiple phyla, each of which subsequently grew larger is indeed a different perspective on the gravity of the CE events.

 

But it does make the "high gravity" event occur much earlier. It sort of kicks the problem back into history a couple hundred million years. And you are also (essentially) asserting that the phyla were not selected.

 

You see the issue?

 

 

Why does all the phyla in the CE have to be descended from one life form? Why not many different protists evolving independently into many different multi cellular phyla? Maybe the real explosion occurred during the "age of protists" over a very long period of time, and only after several different protists evolved into tiny multicellular animals did they start getting bigger with hard parts after the ocean and atmospheric chemistry changed to favor larger life forms? BTW is anyone really saying that 250 million years is too short for phyla to have evolved? Look how Mammals have diversified in the last 65 million years. Yes I know they are all in the same phyla but once the established phyla dominated the Earth development of new phyla became as unlikely as the development of new life forms. The established phyla don't leave niches open long enough for any thing really new to evolve.

[Biochemist]

Why does all the phyla in the CE have to be descended from one life form? Why not many different protists evolving independently into many different multi cellular phyla?

The evidence for common descent is pretty strong. There is a good summary of it at talkorigins.com.

BTW is anyone really saying that 250 million years is too short for phyla to have evolved? Look how Mammals have diversified in the last 65 million years.

Yes. Many have noted that the 250 million year window is VERY short if we expect to see 65+ new body plans materialize via mutation. I have posted a probabilistic question several times on the problem of getting a single enzyme system live in 250 million years. It is VERY hard to get the probability below, say, 1 in 100 billion. The raw probability (based on random behavior) is on the order of 1 in 10^250th. Given that there are about 10^18 seconds since the big bang, this seems like a big number. Let me know if you want me to dig out a reference to the old thread with the probability discussion.

[Biochemist]

Look how Mammals have diversified in the last 65 million years. Yes I know they are all in the same phyla but once the established phyla dominated the Earth development of new phyla became as unlikely as the development of new life forms.

This is a little at odds with the common view of natural selection. You are suggesting that "suddenly" all niches were filled, hence there was no more selection for phyla, but there was plenty of room for new species? I never heard that view before.

 

It is pretty hard to explain why we got so many phyla at the CE and then NONE since. So it looks like we got 60+ new phyla in 250million years, then none in the ensuing 500 million. Seems odd.

[Thunderbird]

Sorry, FT. I was a little vague. The "problem" often described associated with the CE is that these 70 (or so) phyla "suddenly" arrived on the scene after a mere 250 million years (or so). Previously, there were 3 phyla. After, there were 70. And then 40 (or so) of the 70 died out to the present day.

 

If we were to assert that all 70 phyla (that is, 70 different body plans) pre-existed the Cambrian, then the time window to generate the body plans get even shorter. I thought we were suggesting above that the initial life form rapidly branched into most phyla. It is pretty difficult to suggest that this was a mutation-driven natural selection process if it occurred.

 

 

Yes it is, ether the process was hidden in someway occurring over vast periods of time, or the phyla emerged simultaneously but separately from a common single cell ancestor. This problem needs to be addressed on the time frame... in some estimates within a 5-10 million yr window. The other is geometric disparity of body plans of the phyla at that time.

 

This is an important point... Once you have a basic geometrically oriented body plan it is very stable.

These creatures that showed up had a vast array of body plan orientations. It is nigh impossible to completely reorient the geometry of a body plan though mutations and adaptation in this period of time, therefore these geometric orientations could have possibly formed separately and simultaneously from a common primordial cellular agglomerations,.... though an initial process of geometric crystallization that formed around basic principles of organization. Fluid dynamics, environmental cyclical pulses, structural cohesion and symbiotic cellular responses.

[Moontanman]

The evidence for common descent is pretty strong. There is a good summary of it at talkorigins.com. Yes. Many have noted that the 250 million year window is VERY short if we expect to see 65+ new body plans materialize via mutation. I have posted a probabilistic question several times on the problem of getting a single enzyme system live in 250 million years. It is VERY hard to get the probability below, say, 1 in 100 billion. The raw probability (based on random behavior) is on the order of 1 in 10^250th. Given that there are about 10^18 seconds since the big bang, this seems like a big number. Let me know if you want me to dig out a reference to the old thread with the probability discussion.

 

The probablity of life even occuring is very low unless you see the posibilty that life comes about as a natural chemical reaction when the right conditions are met. Could not the same thing hold true for the other aspects of life? I understand the thoughts behind the need for one ancestor but does that ancestor have to be the single spark of multicellular life? Most if not all protists share a common ancestor, just because the range of firsts was spread over several indiependantly evolved multicellular animals doesn't mean they don't all share a common ancestor, it just pushes it back further than the advent of multicellularism. Possibly for the same reasons new phyla could come into being at that time but not now, several multicellular animals came into being at the same time. Since all eco niches for multicellular animals were blank at that time it could have made the advent of several lines of multicellular animals easier than it could be when multicellular animals were already established and radiating into available niches.

[Moontanman]

This is a little at odds with the common view of natural selection. You are suggesting that "suddenly" all niches were filled, hence there was no more selection for phyla, but there was plenty of room for new species? I never heard that view before.

 

It is pretty hard to explain why we got so many phyla at the CE and then NONE since. So it looks like we got 60+ new phyla in 250million years, then none in the ensuing 500 million. Seems odd.

 

You hear something new every day, think about what i am saying. I didn't say new phyla were impossible. I said that any available niches would be rapidly occupied by already established phyla instead of new phyla evolving.

 

It's not at all hard to explain the lack of new phyla if you see that any new phyla evolution would be severly handicapped by competing with already established phyla. Once eco niches were covered by established phyla where would a potintial phyla come from and how could it compete with already established phyla. Yes new niches do open up but not long enough for new phyla to evolve before old phyla simply occuppy the new niches, much less evolution is required for this to happen.

[modest]

Look how Mammals have diversified in the last 65 million years. Yes I know they are all in the same phyla but once the established phyla dominated the Earth development of new phyla became as unlikely as the development of new life forms.

This is a little at odds with the common view of natural selection. You are suggesting that "suddenly" all niches were filled, hence there was no more selection for phyla, but there was plenty of room for new species? I never heard that view before.

 

I believe he is suggesting (and this is a point I've made before) that any new niches that could be filled would more likely be done by the mutation of a species in an existing phyla.

 

If the niche is for a large, aquatic, air-breathing, plankton-eating, warm-blooded animal then it will be easier for a hippo to fill that niche via mutation into a whale than for a sponge to do so. The tree of life builds on itself. The progenitor of modern phyla is extinct - probably outclassed by its own offspring. Why would we expect this extinct animal to keep making new body plans today after the most successful body plans have already been selected and improved upon? It isn't a logical objection in my view.

 

-modest

[Biochemist]

Let me know if you want me to dig out a reference to the old thread with the probability discussion.

 

This discussion is an attempt to quantify the probability of a series of mutations driving development of a single enzyme system. The Cambrian Explosion probably required dozens (or hundreds) of new enzyme systems, but this is the arithmetic to get a single new enzyme system via serial mutation.

 

Originally Posted (withe a couple modifications) by Biochemist, from "Punctuated Equilibria Theories", post #44

Let me start by saying that we understand a relatively small portion of intracellular biochemistry. Like most sciences, the new things that we learn in biological sciences always raise more questions than they answer. This is dissimilar to physics, where leading physicists will actually openly discuss having a "theory of everything" and some will contend that string theory (even though still open to evaluation) is that theory.

 

There is no such position in biochemistry. Every additional material discovery surfaces other issues that bump up intracellular complexity by another order of magnitude. With that preamble, let me bore you with 12 steps of biochem 101 for a second, and then pull out some of the anomalies.

 

 

 

1. DNA is a sequence of four nucleotides (guanine, cytosine, adenine, thymine)
   
2. Three nucleotides in a sequence form a codon. Each of the 64 possible codons "codes" for one of 20 amino acids.
   
3. There are an infinite number of amino acids possible in chemistry. Only 20 are used in living systems- pretty much the same 20 irrespective of the life system. Amino acid anomalies are extremely rare.
   
4. DNA only codes for RNA, and RNA codes for proteins. Proteins are the little machines to do things. RNA pretty much only helps to "transcribe" the DNA to make the proteins. Everything that is done in the cell is either done by a protein, or done by something built by a protein.
   
5. DNA is hence a little machine that builds machines (ribosomes) that build machines (proteins) that build machines (everything else). Since DNA builds itself, you could add at least one more generation on this sequence.
   
6. A typical protein is about 300-400 amino acids. They range from probably about 50 to over 10,000, but 300 is a good average. The set of codons that code for a protein is a gene. Ergo, a typical gene has 300x3 DNA bases in it, or about a thousand.
   
7. Most proteins are highly specific. In most proteins (that have been tested) most individual amino acid residues cannot be changed at all or the protein stops functioning. Most proteins have exactly one substrate, exactly one output, and several speed modulators that control the rate at which the protein functions. Proteins that are acting in this fashion are called enzymes. This is differentiated from proteins that are part of our mechanical structure.
   
8. Proteins are manufactured in a single-thread long string, but this 300 amino acid residue string "folds up" into a ball. It has to be in exactly one ball shape. Most proteins (all?) could fold up into different ball shapes which would be dysfunctional. They usually don't because other proteins ("chaperone proteins" ) manage the fold-up of the new protein to keep it the correct shape. Some diseases are thought to be errors in fold-up (e.g.,Alzheimers, cystic fibrosis) more about that issue at:http://www.faseb.org/opar/protfold/protein.html
   
9. Human DNA is about 3.6 billion nucleotide bases, but there are thought to be only 30,000-40,000 functional genes. Even if there were 100,000 functional genes, that would account for 100 million bases. The other 3.5 billion are just standing by. That is, the ratio of stand-by DNA to functional DNA is probably higher than 40:1. More on that here:http://www.biology.eku.edu/FARRAR/gen-prot.htm
   
10. Most proteins do not act alone. They act in a defined sequence of actions. Glycolysis, the Krebs cycle, the urea cycle, beta oxidation of fats: All of these are multi enzyme processes where the output of one enzyme is the input to the next. I will use the Krebs cycle as an 8-enzyme example (just because it it so famous). Picture here:http://www.bmb.leeds.ac.uk/illingwor...abol/krebs.htm
    
11. Most proteins systems need to be physically associated with each other to function. Hence, there are specific transport systems that transport proteins to their work site within the cell. These transport systems need to recognize the protein and "know" its appropriate location.
    
12. Enzymes occasionally break, or need to fluctuate in quantity. When they do, the DNA is triggered to produce more of the enzyme. A typical human chromosome is about 78 million bases, and is folded at least ten times (into at least a thousand parallel threads of DNA). The DNA is triggered to "unfurl" just a small portion of base pairs, "unzip", and let the messenger RNA transcribe it, move to the cytoplasm, get retranscribed by ribosomes, and make a new protein. The new protein is then chaperoned into a ball, transported into location, and usually inserted into a specific location in the target machinery.
    

Now the math:

 

Granted, the math I will present is related mostly to the human genome. Frankly, at the level of detail we are talking about, it would apply pretty well to bacteria as well. Bacteria don't have genomes quite so big, and have substantially less non-coding DNA (maybe 10% versus human 98%) but the numbers are still impressive.

 

1. To get a functional protein by mutation: you would need at least 200 specific amino acids in specific sequence out of 300 in the protein (it is actually more like 260 on average, but I am making it simpler). This would be randomly 1 in 20^200, or about 1 in 10^260. Heck. To be conservative, let's make it a couple of trillion trillion trillion trillion times more likely, and make it 1 in 10^200.
   
2. Proteins do not work alone, so figuring 5 enzymes in a sequence (being conservative, typical is 6 to 8), this give us 1in 10^1000.
   
3. Keep in mind that there are thousands of separate interdependent enzyme systems and structural construction systems. I am not including the calculations for other logically required systems. Any additional required system would be a multiplier (yes, that would be 1 in 10^1,000,000). Sheesh.
   
4. I have no idea how to calculate the odds of a chaperone protein, since we would have to know the odds of a specific protein folding incorrectly without one. Let's give this one a pass.
   
5. I have no idea how to calculate the odds of recognition in the protein transport systems. We would have to know the requirment for transport, versus the degree of activity if the enzyme system was floating freely. Heck. Let's give this a pass too.
   
6. I have no idea how to calcualte the feedback loop for production of additional protein from DNA, but this one probably dwarfs all of the previous numbers. Remember that we have to expose the specific thread of DNA to let the messenger RNA transcribe it. The DNA unfurls on signal, and this means that one single loop of perhaps 1000-2000 codons out of maybe 70-80 million bases in a chromosome is exposed. I didn't mention that related enzymes are often associated in adjacent genes (called an "operon") and are transcribed as a set, rather than as a single enzyme. I already accidentally gave us a pass for the probability of 5 or 6 adjacent genes of 1000 codons being arranged together on a string of 80 million bases (about 25 million codons). But the real problem is that ANY mutation to the chromosome would tend to mess up this complex unfurling arrangement. So we have to allow for not just the 1 in 10^1000 problem of a mutation to create the enzyme system, but we have to make sure any of the series of mutations to establish the enzyme system does not mess up the feedback unfurling of several thousand OTHER genes on the same chromosome. No guess for the odds here.
   
7. We have not yet discussed the "lysosome problem". Cells are remarkably efficient scavengers, in that they destroy useless junk routinely. This means that the lysosomes (or other scavenger pathways in lower lifeforms) recognize foreign from non-foreign chemicals. This means that a new random protein would likely get scavenged. If it didn't, the cell would be swamped in non-functional proteins. I can't find any information on the efficiency of the cell scavenger process, but certainly a minority of proteins in the cell is non-functional. Otherwise, an organism would spend most of its energy (and food consumption) on production of non-functional material. Clearly not the case. Even if we assume that every 1 in 10^6 mutations was functional (a ludicrously positive assumption) we have to assume that lysosomes destroy the vast majority of these. The lysosome has to recognize these as non-foreign to let them remain. For each enzyme in the sequence. This would be mandatory, or the house of cards falls apart.
   
8. I brought up bacteria above, and that they have perhaps 10% non-functional DNA. Using them as examples of prokaryotes, it sure is odd that these archaic, simplistic systems are so efficient. Is it odd that the progenitors are so genomically efficient and yet the sophisticated, higher systems are not? If we have systems to reverse mutations in DNA (we do) and to eradicate foreign proteins (we do), why don't we have systems to eradicate nonfuncitonal DNA? My suggestion is that we probably do. I suggest this "non-coding" DNA is not nonfunctional. It is required.
   

Anyone who wants to advocate improved morphology by mutation has to get the 1 in 10^1000 number (not to mention the 1 in 10^1,000,000 number) down to something like 1 in 10^6 to 1 in 10^8 to make it have any chance of playing a role in speciation. As a biochemist, I have no idea how do do that intelligently.

[Moontanman]

I believe he is suggesting (and this is a point I've made before) that any new niches that could be filled would more likely be done by the mutation of a species in an existing phyla.

 

If the niche is for a large, aquatic, air-breathing, plankton-eating, warm-blooded animal then it will be easier for a hippo to fill that niche via mutation into a whale than for a sponge to do so. The tree of life builds on itself. The progenitor of modern phyla is extinct - probably outclassed by its own offspring. Why would we expect this extinct animal to keep making new body plans today after the most successful body plans have already been selected and improved upon? It isn't a logical objection in my view.

 

-modest

 

Yes! Exactly!

[Moontanman]

Yes but all that is moot if the strcture for multicllular life were already in place in the protists. And this is the case, all it took was a reshuffle of traits already present to bring about the more complex but still tiny multicellular animals which were already preadapted to growing larger when conditions were right. If chemical and physical conditions had never changed to favor larger animals we could still be living on a world with nothing but many tiny multicellualr animals. (well we wouldn't be living here but they would) Everytime we see a new surge forward towards complexity it is accomponied by environmental changes that allow it to happen. Evolution isn't the history of new mutations suddenly changing life it's the history of life using existing genes in different ways. Mutation might make it possible but the driving force is the environment. Eukarotes were already growing towards the traits that made protists possible beofre protists came into being, protists were already using genes to express things that could be used in different ways to allow multicellular animals to exist. Tiny multicellualr animals were already preadapted to be larger and became so as soon as conditions allowed it, hard parts soon followed for the same reasons.

[Biochemist]

I believe he is suggesting (and this is a point I've made before) that any new niches that could be filled would more likely be done by the mutation of a species in an existing phyla. ....The tree of life builds on itself. ...It isn't a logical objection in my view.

I am OK with this hypothesis. I just never heard it before. I frankly can't see any obvious reason why we would not see more phyla (in addition to more species) but I can accept the hypothesis that (somehow) some species gained dominance and essentially crowded out other new-phyla interlopers.

 

Love that word, "interloper".

[Biochemist]

The probablity of life even occuring is very low unless you see the posibilty that life comes about as a natural chemical reaction when the right conditions are met....

That is the problem we are trying to quantify. In the post above, we took a VERY simple extension to an existing life form (with patent, functional DNA and all intracellular machinery already in place) ans asked the question: What are the odds that we could add a single enzyme system to this entity.

 

And the number comes out astronomical, even under incredibly favorable circumstances.

 

It is just hard to rationalize a "mutative" solution to tis problem, particularly in the case of the 250 million year window in the Cambrian Explosion.

[Thunderbird]

Anyone who wants to advocate improved morphology by mutation has to get the 1 in 10^1000 number (not to mention the 1 in 10^1,000,000 number) down to something like 1 in 10^6 to 1 in 10^8 to make it have any chance of playing a role in speciation. As a biochemist, I have no idea how do do that intelligently.[/i]

 

 

Got it...... now instead of going over the same debate that goes on and on, on every science forum and never ever gets anywhere because of the information you just gave. instead address post 344. As this scenario I gave eliminates the genomic constraints.

[Biochemist]

Got it...... now instead of going over the same debate that goes on and on, on every science forum and never ever gets anywhere because of the information you just gave. instead address post 344. As this scenario I gave eliminates the genomic constraints.

I really don't mean to avoid your question, TB. I just really don't understand anything about how this addition avoids the genomic constraints. I might not be smart enough to understand what you are saying. But I just don't see how the structural stuff you mentioned in post 344 does anything to mitigate the complexity of genomic "improvements" over time.

[Thunderbird]

I really don't mean to avoid your question, TB. I just really don't understand anything about how this addition avoids the genomic constraints. I might not be smart enough to understand what you are saying. But I just don't see how the structural stuff you mentioned in post 344 does anything to mitigate the complexity of genomic "improvements" over time.

That's because you are stuck with genomic constaints its really simple like I have said many times now This has nothing to do with genomic constraints. It is prior to the multi-cellular organism.

[Pyrotex]

[Woops! I think I posted in the wrong evolution thread]

 

Consider that biological evolution was never intended to reflect un-natural selection, culture, war, medicine, acts of Man or any other process shorter than geologic time.

 

It was specifically constructed to answer the questions of how and why did animals and plants appear to change over geologic time. This is not a "weakness" or "failing" of the theory of evolution.

 

It's like trying to apply the theory of fixed wing aircraft to a bumble-bee. It will give you the wrong answers. It wasn't meant to apply to moving wing aircraft on the scale of insects. The theory works fine for the domain for which it was constructed.

 

The theory of evolution works fine for the domain for which it was constructed.

[Thunderbird]

I just goggled "stem cell Cambrian explosion" to see if anyone is investigating this same scenario.:rolleyes:

 

 

 

 

 

What triggered the Cambrian Explosion?

 

 

Almost all of today's animal body types evolved in a single period less than ten million years long. This "explosion" of diversity occurred with seemingly random timing in a period tens of millions of years long. The abruptness of the Cambrian Explosion was a severe puzzle to Darwin, and has remained troubling ever since.

 

 

 

Why did the Cambrian Explosion happen when it did? If it was so abrupt--just waiting to happen--why didn't it happen earlier? Chris Phoenix thinks he knows the answer.

http://http://bilconference.pbwiki.com/Cambrian+Explosion

 

 

585 million years ago (MYA), the earth was heavily glaciated, and life (as far as we know) had not progressed past the single-celled stage. By 575 MYA, the first multicellular fossils have been found. But the Cambrian Explosion waited until about 545 MYA.

 

 

 

There were, of course, several enabling factors, such as the retreat of glaciation, the increasing oxygen content of the atmosphere, and the gradual complexification of organisms. But all of these were slow processes, or else predated the Cambrian Explosion by tens of millions of years.

 

 

 

It seems likely that there was a trigger intrinsic to organisms--some capability that developed in some lineage, that took time for evolution to discover, but that was highly advantageous once it arrived--advantageous enough to allow that lineage to diversify wildly, and to outcompete many other lineages.

 

 

 

Cellular differentiation--the ability of a cell to lock itself into a particular specialized type, without requiring ongoing chemical signaling--is proposed as a suitable trigger for the Cambrian Explosion.

 

 

 

Jellyfish and hydras, which predate the Explosion, have cells that are specialized but not differentiated. Differentiated cells would allow intricate multi-scale structures--organs and networks--to be maintained with far less energy cost. However, differentiation would be a losing proposition for single cells, so would have taken a while to evolve.

 

 

 

The differentiation hypothesis also has implications for embryology and stem cell research