Punctuated Equilibria theories

[ldsoftwaresteve]

I'll be dipped. If this is what I think it is, it seems in line with what I've always thought: Creationism and gradual evolutionism are both wrong. Creationism ignores ancient evidence and gradual evolutionism plays dice with very long odds and doesn't account for many new species in a short period of time. Evolution happens in spurts.

Correct me if I'm wrong (like you won't?), but are you saying that some event comes along and reshuffles the genetic deck to the next stable configuration? The implication being that the next series of stable configurations are a 'higher' form of life? Any idea what the form of stress happens to be? Is it a blast of radiation or just starvation?

Also, this would not contradict what James Putnam has been saying.

[gubba]

G'day folks,

I just lost my entire post bar the last few words, yet again! You'd think even an old geezer would become proficient in the end! Oh well, Too bad.

Buffy I'm afraid you'll have to put up with me on your side. I can't help emphasising the critical importance of your appreciation of the length of time and number of generations involved when considering evolution. When talking of species we're dealing genetically with god knows how many powers of magnitude of readings of the four letter code. Your neat little - cop going nope, nope,... - example passes Ockham's for me. By the way anyone know any solid, recent update on PE especially in reference to that so called fossil record.

Bio and bumab, I'm a bit bemused with your difficulty re viable mutations. Are you saying new species equals new proteins? I've been led to believe this isn't at all essential, just variations in the usage of protains etc. will ensure vast change. Bio, would you care to estimate the order of magnitude of the readings of our genetic code that makes up our lives, elsewhere I've already owned up to my arithmetical failings. It is this reading of our codes that helps us to self-repair as you have noted but this ability enables adaptation as well as species statis surely?

Perhaps it pertinent at this point to restress the role of natural selection or, if you prefer, the environment in ordering speciation. I view current species as current viable possibilities, we are all potentialities responding, interacting with the world other than us. Stable environment, stable species, varying conditions diferentiation within species etc. The range of variation within species can be considerable, surely ideally placed to try out any new niche that may open? The proponents of gradualism I respect never claim some form of smooth, steady pace of incremental change.

Bio, re. your theory and my simple question in my last post. I'm bemused that you're not happy with the second prokaryote as our ancestor. After all doesn't 3 odd billion years of how many generations of single celled existence create the opportunity for the incredible genetic complexity that took multu-cellular life with such gusto? cheers gub.

[Biochemist]

Originally Posted by ldsoftwaresteve

...are you saying that some event comes along and reshuffles the genetic deck to the next stable configuration? The implication being that the next series of stable configurations are a 'higher' form of life? Any idea what the form of stress happens to be? Is it a blast of radiation or just starvation?...

Rather than just offering conjecture, I would like to stick with what we know. We know, for example, that any sequestered family will tend to incur a higher likelihood of anomalies. This is at least partially due to matching recessive alleles in the children (this is why siblings and cousins can't marry). But there could be other mechanisms as well. Hence, we may not know all of the mechanisms for the sudden morphological change after a family is sequestered, but we see it in most species, including humans.

Ergo, we have a known effect of dramatic, viable morphological change in sequestered families. Cataclysm would cause a large number of sequestered familes in many species concurrently. That is my suggestion, based on the observations that we have, for the main mechanism of speciation. And this has almost nothing to do with serial mutation.

Notably, this mecahnism does not require a cataclysm. A cataclysm just tends to raise the likelihood. This model matches the fossil record.

[Biochemist]

Hey, I empathize with your loss of posts, Gub. I have lost several myself.

Originally Posted by gubba

....Are you saying new species equals new proteins? I've been led to believe this isn't at all essential, just variations in the usage of protains etc. will ensure vast change. Bio, would you care to estimate the order of magnitude of the readings of our genetic code that makes up our lives, elsewhere I've already owned up to my arithmetical failings. It is this reading of our codes that helps us to self-repair as you have noted but this ability enables adaptation as well as species statis surely?

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 proteins and RNA. 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 ribosomes zip along it the 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 ribosomes zip along 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.

Too long an answer to your question. But 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.

Perhaps it pertinent at this point to restress the role of natural selection or, if you prefer, the environment in ordering speciation. I view current species as current viable possibilities, we are all potentialities responding, interacting with the world other than us. Stable environment, stable species, varying conditions diferentiation within species etc.

Agreed. All we are talking about is "How?"

Bio, re. your theory and my simple question in my last post. I'm bemused that you're not happy with the second prokaryote as our ancestor. ...

I actually have no problem with the second prokaryote. I just picked the older one to give us more time. I have no fact basis to pick one over the other.

[ldsoftwaresteve]

Thanks BIO, Bumab, Buffy et al (hmmm, lots of Bs there) - Nice thread guys. And I can understand Buffy's idea of mutations lying dormant until a stress situation appears. Really excellent work. Damn.

The effect of all of this is that my model is collapsing (I've been wrong - well, sort of right for the wrong reasons, but still wrong!). What a hatefull thing to have to admit. I have to assess the damage.

@#$&!

[ldsoftwaresteve]

Just read your 101 post BIO and I want to thank you for the synopsis. Quite interesting.

Is there any chance that we aren't dealing with a random set of events in the actions where the pieces combine to make new configurations? Specifically, is there any evidence to suggest that something like another property, so far undetected, is stacking the deck? Something akin to feedback by an organisms surroundings which presents the nature of those surroundings as a sort of 'guide'?

[Biochemist]

Originally Posted by gubba

...Bio, re. your theory and my simple question in my last post. I'm bemused that you're not happy with the second prokaryote as our ancestor. After all doesn't 3 odd billion years of how many generations of single celled existence create the opportunity for the incredible genetic complexity that took multu-cellular life with such gusto?

One more point on the math in this. 4 billion years is only 10^14 generations assuming an average generation is 20 minutes (using an E coli as our average generation time) which I suspect is being gracious. I am not sure how to estimate how many serial mutations are necessary to get from our abiogenic prokaryote to humans, but it is at least one for each of our 40,000 genes. I suggest 100,000 mutations is pretty conservative (I think a million to 100 million is more likely). At 100,000 mutations, we would have to have a positive, retained mutation every billionth generation. Most arguments to explain retention suggest that the systems are incrementally valuable, This would significantly increase the number of positive mutations required to establish a "selectable" mutative path. If it took 100 interim viable steps for each human gene, that would be about 10 million positive mutations, or 1 positive, retained mutations in 10 million generations (still assuming a generation is 20 minutes).

And that assumes even, gradual mutation, which it at odds with the fossil record. I think the arithmetic here is untenable.

We do get demonstrable morphology changes in E coli (under stress) in about a thousand generations. This is the link that Buff posted from Scientific American that showed a sudden 30% increase in cell size. But this is reproducible, so my contention is that this is not a mutation. It is codified in the E. Coli genome.

[Biochemist]

Originally Posted by ldsoftwaresteve

Is there any chance that we aren't dealing with a random set of events in the actions where the pieces combine to make new configurations?

The core of my hypothesis is that none of this is random. All speciation events (well,the vast majority) are specified in the code of the parent species. That way, you can get significant morphological change in as little as one generation.

... is there any evidence to suggest that something like another property, so far undetected, is stacking the deck?...

We have already bought up several in this thread. Empirically, the fact that speciation tends to bunch around cataclysms argues against gradualism. Further, we have many examples of known, recurring morphological anomalies that occur in a single generation. I have argued that if they recur, they are not mutations. They are likely outcomes, based on the code of the parent. Examples like trisomy 13 (Downs syndrome) , or the cases where insects or amphibians get extra legs in a single generation are examples of likely, recurring anomalies that are codified in the parental species DNA.

[Biochemist]

Originally Posted by gubba

...doesn't 3 odd billion years of how many generations of single celled existence create the opportunity for the incredible genetic complexity that took multu-cellular life with such gusto?.

OK, last one on this.

The first mammals are thought to be the small shrews that arrived at the beginning of the Triassic period. This is about 250 million years ago. Most of these species will probably have generations that are more like a year, hence 250 million generations. They also have far smaller "litters" than lower life forms. If we assume (generously) 10 viable mutations in series for each functional human gene to get from the Triassic shrew, that would be 250,000,000 generations /(40,000 genesx10 serial mutations) = one successfully updated gene every 625 generations. This means that we now have to get retention of genes every 10^3 generation in the species that are most likely to reject foreign substances. It would also imply a new hominid (genetically) about every 10,000 years, assuming 15 year generations. That would be a bunch of differnet hominids.

Hmmmm.

[ldsoftwaresteve]

Sorry BIO, I don't mean to appear dense (and perhaps can't help that), but I was not referring to the parent genes. Is it possible that outside environmental factors are directly manipulating reorganization through some property we cannot, as yet, detect? Or, are you saying that something in the makeup of the parent genes is receptive to large change?

Perhaps both? That would seem to imply a direct influence between environment and genetic makeup. That would also seem to imply a sort of awareness of environment at the genetic level.