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Evolution: the Facts.

dgilman said:
Here's another:
If the subset is too tiny, then the subsequent inbreeding eventually results in infertility or a heavy load of mutations that severely prejudices their viability. That condition is currently being faced by pedigree pet breeders.
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Dinwar already explained the major flaw here, but let me add a bit more: pet breeders have a habit of selecting for the wrong traits. An unfortunate number of breeders are trying to create show-quality dogs that meet certain aesthetic standards, which are sometimes directly at odds with what would be good for the animal's health. Pugs, for example, are bred to have that trademark flat nose--even though it causes respiratory issues. The problem isn't merely that pugs are being inbred with more pugs, but that pugs which have an unhealthy trait are being bred with other pug who share the same unhealthy trait, for the express purpose of propagating that trait. So it's not really fair to say that purebred dogs show the problems with inbreeding, because you're looking at a stacked deck.

Each development by series of mutation must be independent of each other yet result in full cooperation and they must synchronize with each other.
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Of course, any mutations which don't work have a greater chance of being weeded out through natural selection, meaning that you are again looking at a stacked deck.
 
Akri said:
Of course, any mutations which don't work have a greater chance of being weeded out through natural selection, meaning that you are again looking at a stacked deck.
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Any EXPRESSED mutations that don't work. However, going from the genetic code to the phenotype is extraordinarily complex--gene expression is an entire field of biochem in and of itself, one which I do not pretend to understand (it's all squishy, and none of it generally lasts more than a few thousand years). However, I know off the top of my head two situations where a gene can do whatever it wants, with absolutely no restrictions: female x chromosomes in mammals, and double-crossovers.

In many female mammals one x-chromosome is either entirely dormant or is only partially expressed, to prevent doubling the dosage of various chemicals. This is why certain cat patterns only occur in female cats--which x chromosome goes dormant is random, and coloration is coded for in that chromosome. The dormant gene can have all kinds of mutationos in it without doing anything to the animal.

Similarly, if a gene experiences duplication due to a double-crossover and is unexpressed for some reason (not unlikey, considering the odds of getting the entire gene in a single double-crossover event) the gene can undergo any mutations in the world, even coding for lethal proteins, and it won't do anything at all to the organism. If the gene becomes active again (another mutation or cross-over adding a start or stop codon to it, for example) it can do remarkable things. This is, for example, one way to get irreducible complexity in organisms (not a common way, but it's a viable pathway).

Then there's ontogeny to consider. Much of natural selection occurs before the organism is even born--if the genetic code isn't viable the organism will fail to develop, or spontaneously abort, or otherwise fail to come to full term. Any molecular analysis of evolution that doesn't include ontogeny is necessarily flawed and biased.

I don't mean these as corrections to your post, Akri; they're intended more as an expansion on the point.
 
Sad thing is, I'm doing this to relax after spending all day looking for fossils in a desert 10 hours a day. I should get some serious nerd-cred for this. :D
 
As for sexual selection being something that is inexplicable and needing large amounts of interdependent mutations.

In addition to Dinwar's links I'd like to draw your attention to this article on wiki and its accompanying literature:
http://en.wikipedia.org/wiki/Bacterial_conjugation

In a nutshell, a tiny independent segment of DNA can get bacteria to transfer DNA from one intact cell to another without division occuring. Such a mechanism would make an excellent basis from which to evolve sexuality. I'm not claiming it happened that way, as there are probably dozens of different theories on how such a thing can evolve, but that is quite the opposite of the claim that it's impossible to ever find out.
As with many parts of the theory of evolution the trick isn't finding a possible mechanism on how X can occur, but rather finding out which of the many logically possible ways actually happened.
 
". . . when you say "diversity" get's smaller that's untrue" I am now wondering about my English.

The total number of genetic variations and the total number of genes of the subset population is drastically less that what exists in the original population. I grew up on farms. That loss of diversity was always a problem. The farmers' only recourse in those days was to introduce "wild" strains or to import stock from overseas to interbreed with the local stock. Mutations just did not do the job and in fact endangered the viability of the animals or the fields.

The theories to explain how unicellular organisms may have evolved into multicellular ones are very logical, but I have yet to see anything to demonstrate why I should believe that what the theories say is what had actually occurred. I have even asked persons with PhD's to show me why I should. Most have not answered and the one who did has expressed doubts. In an article I read on the problem the author indicated that none of the examples used in the theories addressed the problem of getting the necessary information into the genes of the gonad cells.
 
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". . . with many parts of the theory of evolution the trick isn't finding a possible mechanism on how X can occur, but rather finding out which of the many logically possible ways actually happened."

That is the vexing problem I'm having with it. The other is that in too many cases, observation do not corroborate the theory and way too often contradicts them.
 
dgilman said:
I grew up on farms. That loss of diversity was always a problem.
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Well, there's your problem. You're assuming that the natural environment necessarily always functions in the same way as a farm. It does not.

The number of individual genes may be smaller, but the number of variations may or may not be. What IS a problem is that statistical fluctuations can lead to rapid fixation of genes, regardless of whether they're beneficial or not, in small populations. It's not the lack of diversity that's the problem, fundamentally; it's fixationof deliterious traits.

And I grew up helping out on a farm as well. I have a fairly good sense of what I'm talking about, after observing it in barn cats.

The theories to explain how unicellular organisms may have evolved into multicellular ones are very logical, but I have yet to see anything to demonstrate why I should believe that what the theories say is what had actually occurred.
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This is starting to sound like "Were you there?" What specific evidence would convince you? Please be as specific as possible; I'd really rather not waste both of our time.

I will, however, point you again to the walking bryozoan collonies. These exhibit specialization that's somewhere between a collony of animals, and one super-organism--like, some animals in the collony are specialized for reproduction, while others are specialized for locomotion. You'll find some good parallels with the unicellular/multicellular transition reading up on that.

I have even asked persons with PhD's to show me why I should.
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What field were they in? A dinosaur expert would certainly not be able to tell you. An invert K/Pg guy would likewise be unable to. Merely having a Ph.D. does not make one an expert in all things.

In an article I read on the problem the author indicated that none of the examples used in the theories addressed the problem of getting the necessary information into the genes of the gonad cells.
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That guy's an idiot, pure and simple. All cells have the genetic information necessary to reproduce. We've proven that via cloning--we can re-set skin cells, for example, as stem cells. There is NO problem, AT ALL, with getting the necessary information into the genes of hte gonad cells. As soon as the cells split, the information is there.

The other is that in too many cases, observation do not corroborate the theory and way too often contradicts them.
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Please provide specific examples. I've seen data that contradict specific theories on specific adaptations and evolutionary lines, but I've yet to see anything that contradicts evolutionary theory as a whole. What I've seen far more frequently are observations misinterpreted in such a way as to appear to contradict evolutionary theory.
 
dgilman said:
". . . when you say "diversity" get's smaller that's untrue" I am now wondering about my English.

The total number of genetic variations and the total number of genes of the subset population is drastically less that what exists in the original population. I grew up on farms. That loss of diversity was always a problem. The farmers' only recourse in those days was to introduce "wild" strains or to import stock from overseas to interbreed with the local stock. Mutations just did not do the job and in fact endangered the viability of the animals or the fields.

The theories to explain how unicellular organisms may have evolved into multicellular ones are very logical, but I have yet to see anything to demonstrate why I should believe that what the theories say is what had actually occurred. I have even asked persons with PhD's to show me why I should. Most have not answered and the one who did has expressed doubts. In an article I read on the problem the author indicated that none of the examples used in the theories addressed the problem of getting the necessary information into the genes of the gonad cells.
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http://www.ncbi.nlm.nih.gov/pubmed/15004568
In this paper there is a detailed analysis of how a simple error in cell duplication, in this case stable full duplication of a genome, leads to two whole different species.

Of course whole genome duplications are rare, but especially in organisms with multiple chromosomes this is a well established and proven mechanism to gain duplicates of essential genes, allowing one of the copies to mutate without loss of function. This 'creates' new information over time

This of course still neglects horizontal gene transfer, sym/endobiosis, intron gain, crossovers, viral gene transfer, natural electrotransformation at lightning impacts and probably several other ways in which DNA can be stably added to a cell/organism.

However, the timescale of speciation is in the hundreds of thousands of years, whereas your example of a farm doesn't even scratch the surface of such era's, as farming itself is less than a percent of the needed time old.
 
dgilman said:
The total number of genetic variations and the total number of genes of the subset population is drastically less that what exists in the original population. I grew up on farms. That loss of diversity was always a problem. The farmers' only recourse in those days was to introduce "wild" strains or to import stock from overseas to interbreed with the local stock. Mutations just did not do the job and in fact endangered the viability of the animals or the fields.
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That's incorrect unless you're referring to breeding programs where you artificially restrict gene flow and even then the variation is still probably high. The problem with breeding is that particular QTL's which are selected for are often bred to over express particularly with regards to dogs breeds (an honest opinion: I abhor dog breeding programs in some respects). This is not a fair standard to hold evolution to as in nature the variation increases. Artificial selection is a pressure that's very specific and very direct.

If you think about it, evolution does a better job of explaining diversity and if you adopted creationism then you'd be stuck with your artificial selection problem even more. It's a stronger proof against creationism.

Mutations are not the sole factor of variation but they're a great factor novel and enhanced expression. They happen so often and so many times per individual that their effect is beyond question. But when you artificially select for QTL's you fix some alleles for QTL's that may not produce strong fitness in nature which becomes irrelevant in an artificial environment which is why you can see it in farms and breeding programs. In a spatial model genetic variation will still be high but limited to QTL artificial selection.

I need to mention again is that subsetting the original reduces variation by fixating alleles quickly, either to the benefit or detriment of the subset population. BUT that in and of itself acts as a selection pressure which allows for variation that differs from the "original population" anyways. In a sense you WILL get increased variation given that the subset population doesn't go extinct. This is how nested heirarchy populations produce new species (or at least one of the ways anyways; you can get speciation in other methods too). Again spatial modeling shows a propensity for increased variation, it's just that increased variation doesn't trend towards increased fitness (ie. negative alleles lower fitness and are selected against generally, neutral alleles or nearly-neutral alleles have no observable effects yet, and positive alleles will trend toward fixation) because the variation means dick-all without a continuum and selection factors. That's why spatial stochastic modeling provides a more robust description for the observed phenomenon.
 
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dgilman said:
The theories to explain how unicellular organisms may have evolved into multicellular ones are very logical, but I have yet to see anything to demonstrate why I should believe that what the theories say is what had actually occurred.
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Two reasons:

1. We have today a great diversity of life forms in our biosphere, and

2. Evolution by natural selection is the only plausible mechanism by which this can happen.

In case that's not enough, here is a third one:

3. Every significant prediction made by evolutionary theorists has proven to be correct. Most importantly, genetic structure, which was only dreamed about in Darwin's time, has lined up perfectly with expectations.
 
Speaking of Ph.D.'s not necessarily being useful outside one's field, this seems to me like a wrong interpretation of evolution. Can any of our resident experts tell me if my intuition is correct?
 
Prometheus said:
Speaking of Ph.D.'s not necessarily being useful outside one's field, this seems to me like a wrong interpretation of evolution. Can any of our resident experts tell me if my intuition is correct?
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In my short, inexpert opinion, there is a valid concern raised, but the claim at the end for why things are the way they are just doesn't work.
 
Prometheus said:
Speaking of Ph.D.'s not necessarily being useful outside one's field, this seems to me like a wrong interpretation of evolution. Can any of our resident experts tell me if my intuition is correct?
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The whole idea that evolution works towards some form of 'better' species is wrong.
Slapdash 'eh. good enough, lets call it a day' would be a far better analogy.

The concept that death exists so that newer things can flourish is post-hoc argumentation too. The very nature of DNA ensures that eventually errors will occur and with enough errors it stops working. It's impossible to keep that from happening, but you can make lots of copies to limit the effect.
 
Lukraak_Sisser said:
The whole idea that evolution works towards some form of 'better' species is wrong.
Slapdash 'eh. good enough, lets call it a day' would be a far better analogy.

The concept that death exists so that newer things can flourish is post-hoc argumentation too. The very nature of DNA ensures that eventually errors will occur and with enough errors it stops working. It's impossible to keep that from happening, but you can make lots of copies to limit the effect.
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First off the argument has to be made that the gene(s) that cause senescence benefit themselves. Then it can become a competition between longevity of reproductive life time and clearing unreproductive individuals from competition.
 
Lukraak_Sisser said:
(snio)...
The very nature of DNA ensures that eventually errors will occur and with enough errors it stops working. It's impossible to keep that from happening, but you can make lots of copies to limit the effect.
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Yes, but some cells are programmed for cell death (such as those between the fingers when the hand is just a club). Apparently the rest of our cells are also programmed for cell death at our old age. I stand to be corrected.
 
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