Natural selection is a guided process, guided not by any higher power, but simply by which genes survive and which genes don't survive. That's a non-random process. The animals that are best at whatever they do"”hunting, flying, fishing, swimming, digging"”whatever the species does, the individuals that are best at it are the ones that pass on the genes. It's because of this non-random process that lions are so good at hunting, antelopes so good at running away from lions, and fish are so good at swimming.

Here in the New England is does not pay to be the biggest "baddest" buck. Do you think hunters go after the weak and frail? In Africa it does not pay to be the fastest zebra/ antelope (first to the lioness' ambush).

How many times do accidents (ie chance events) claim the lives of individuals within a population? IOW far from "gloss" Dr. Berlinski's article struck at the heart of the matter. There exist many factors that contribute to the proliferation or demise of an allele, individual and/ or population. Sir Richard would have best said, "the animals that survive long enough and (successfully) mate have the best chance of passing on their genes."

It should also be noted the genes that get passed on do not explain the origin of the organism in the first place. Natural selection can only select from existing qualities. It cannot explain the origins of those qualities. Oscillation of allele frequencies can be explained by NS. Genetic homeostasis can also be explained by NS. IOW NS has all the appearance of a conserving force, just as Blythe told us some 170 years ago.

I'm not sure I had an "objection" to NS. My first post was about Sir Richard claiming that NS was a "guiding force"- that was from the same guy who told us that NS is blind and purposeless.

How many guides do you know who are blind and without purpose?

"That non-randomness of natural selection is why Dawkins objects to claims that evolution is wholly random."

I apologize that I haven't followed the entire thread closely, but the "non-randomness" of evolution is only trivially due to natural selection. We know that evolvability is a quality of variation, so the non-randomness in evolution is due primarily to non-randomness in variation. We know this through empiricism. The Darwinian algorithm is often impotent. This is known as the representation problem in evolutionary computation. The solution to the representation problem was the creation of the genotype-to-phenotype map. The map itself creates evolvability, and different maps create evolvability with different trajectories. This is all independent of Natural Selection; Natural Selection does NOT shape potential evolutionary trajectory; it actualizes existing potential. So yes, in this sense NS provides directionality (non-randomness), since nature selects the roads to travel. But the roads were paved by evolvability, which again, is a quality that absolutely depends upon variation. This is why bibod is correct when he says upfront:

"In other words, Darwinism has to be committed to the view that the same features that we see today in the biological world would also be produced in an environment with unliminted resources, where all organisms reproduced and passed on their genes. All the novelty that exists today would exist in that environment, plus some."

Selection streamlines evolution, but it is not responsible for it. The nature of variation creates evolvability. And yes, in a thought-experiment world with unlimited resources, and WITHOUT selection . . . evolution still occurs. So to attribute evolution to natural selection is a false attribution.

You claimed that the toxic newts were only a selective pressure if they were the sole food source. But, I agree with your new statement. If the newts are so rare as to be a vanishingly small potential food source, then there would be little or no selection for resistant snakes. How does this help your argument that natural selection does not explain TTX-resistant snakes?

As for how "built-in responses to environmental cues" would work- very similar to computer programming (C++ for example) with its statements such as "if", "else", "while", etc.

I've been giving you examples of real biological systems and arguing in terms how how the animals interact with specific environmental features. You're giving me a vague analogy to computer programming? How, in terms of cellular structures and biochemistry, does "if," "else," and "while" allow a cell to know that making targeted mutations of a sodium channel (as opposed to calcium channels or any other protein) is advantageous in the presence of toxic newts?

As for Occam what are the odds a "random" mutation would come along in just the right locus (loci) to convey an advantage? What are the odds if several mutations are required?

That would depend on the population size, the mutation rate, and the number of generations involved. These are single-nucleotide changes that even the most hard-core young earth creationist agrees are possible. As you point out, the mutation could already be present at low levels in the population before that came in contact with the newts — I have already suggested that these mutations probably occur as rare events in all populations of garter snakes (and in all vertebrates, for that matter). As for the second and subsequent mutations, their probability would be the same as the first mutation, because they would occur in a context where the first mutation has already been selected for.

Also remember that there are multiple potential mutations, not just one, that can render a channel TTX resistant.

The most likely scenario is that the adavantage already existed in the population but that advantage became more prevelant when those without the advantage started to be selected out. How the advantage arose isn't important just that an advantage existed and NS acted on it.

So, we're agreed that Natural Selection could result in increased prevalence of the trait in the population? This takes us back to the beginning of the thread. What exactly is your objection?

But where did that TTX-resistant channel come from originally? Your vague built-in mechanism won't explain it, if it is already present in the population before they encounter toxic newts. Mutation happens — has any other real alternative been proposed?

Nick:
Not necessarily so. In addition to the variety of food sources you also have to consider effective population sizes of those food sources and potential competitors for those food sources. If the newts are toxic to most vertebrates, their population may be quite high relative to other potential snake food. I have seen very dense populations of eastern newts, a related toxic species, in some lakes. So, a resistant snake will have an increased source of food relative to the sensitive conspecifics with which it competes. A sensitive snake will waste relatively more time and energy pursuing prey that it will need to regurgitate and which could paralyze or possibly kill it. If all snakes are sensitive, they are at the same relative disadvantage, but a resistant mutant is not.

You just confirmed what I said. The "selective pressure" is directly related to the population size of the toxic newts in relation to all the other food sources in the area.

As for how "built-in responses to environmental cues" would work- very similar to computer programming (C++ for example) with its statements such as "if", "else", "while", etc.

As for Occam what are the odds a "random" mutation would come along in just the right locus (loci) to convey an advantage? What are the odds if several mutations are required?

The most likely scenario is that the adavantage already existed in the population but that advantage became more prevelant when those without the advantage started to be selected out. How the advantage arose isn't important just that an advantage existed and NS acted on it.

Not necessarily so. In addition to the variety of food sources you also have to consider effective population sizes of those food sources and potential competitors for those food sources. If the newts are toxic to most vertebrates, their population may be quite high relative to other potential snake food. I have seen very dense populations of eastern newts, a related toxic species, in some lakes. So, a resistant snake will have an increased source of food relative to the sensitive conspecifics with which it competes. A sensitive snake will waste relatively more time and energy pursuing prey that it will need to regurgitate and which could paralyze or possibly kill it. If all snakes are sensitive, they are at the same relative disadvantage, but a resistant mutant is not.

And don't forget that the resistant snake has a second potential advantage. It becomes toxic itself if it eats toxic newts.

Not so. Ya see that "built-in" mechanism could be messed up in some individuals due to random mutations.

Are you serious? So, now you have targeted mutations of a sodium channel driven by an unknown "built in" mechanism which is itself affected by random mutations. The alternative is random mutations in the sodium channel which actually mediates the phenotype in question. William of Ockam, paging William of Ockam

Your "built in mechanism" only works if there is actually an advantage to the snakes which are TTX resistant. If you are correct that there is no advantage to resistant snakes, then there is no reason for a "built in" mechanism to generate resistant snakes. If there is an advantage to resistant snakes, then there is no need to an additional "built in" system.

Tell me more about the built in system. How does it work? What is it made of? How does it know which mutations to make in an organism exposed to tetrodotoxin versus one exposed to saxitoxin or pyrethroids? How does it know to mutate a sodium channel gene instead of a calcium channel gene?

So, when you say that we're looking at a mutation that changes the sodium channel that prevents TTX from binding, that's not a creative process. There is no new function, but rather is simply a diversification of of an already-in-place system that understandably affects related process, such as the binding of TTX for one. You ourself seem to understand the implication here when you admit, "So you can only characterize TTX resistance as a "damage" to the genetic material if you have in mind some idealized sodium channel in an idealized environment".

Now, I'm not sure that I would call it the result of 'damage' to genetic instructions at this point — perhaps it is just the slight diversification of it? But toxin resistance at a price of slower movement as a result of mutation is one thing, while a mutation resulting in the evolution of new genetic instructions coding for an enzyme that breaks down TTX with the snake maintaining its speed is another.

Nick:
Your prediction is proven false for a variety of reasons. Garter snakes eat a wide variety of small vertebrates and invertebrates, so no population is wholly dependent on newts.

In that case there isn't any "selective pressure" due to the toxic newts. That was the point (your point) I was addressing- toxic newts being a "selective pressure". They would be only if they are the sole source of food, less so if they are one of very few sources and even less if there is a wide variety of foos sources.

Nick:
1. That in populations of snakes, occasional random mutations generate tetrodotoxin resistance. Those mutations are advantageous in populations that co-exist with newts, and therefore increase in frequency. As a result, we tend to observe resistant snakes in areas with toxic newts.

In scenario two, we should always observe resistant snakes when we see toxic newts, because the "built-in" response will always be present.

Not so. Ya see that "built-in" mechanism could be messed up in some individuals due to random mutations. Also even if the mechanism was intact it may not have been triggered in all individuals for any number of reasons- one being not every offspring inherits every trait that each parent has.

Bricelj et al (2005) Nature 434: 763-672

A single point mutation makes clams resistant to saxitoxin. The kinetics of the mutant channel were tested, and no changes could be detected. The mutation is advantageous to clams in regions with toxic plankton. So, in this case, we seem to have an advantageous mutation (gain of STX resistance) that is not accompanied by any "damage" to another trait.

As Joe points out, NO trait is unconditionally advantageous. Advantage is ALWAYS relative to environment.

Additionally, it would help to know what mutation triggers this resistance. Is it actually a mutation that causes a reduction in relevant neuro-transmitters, for instance? If so, any mutation that causes a reduction in activity or production of anything to cause an "advantage" is only an "˜advantage' in the sense that such is gained as a result of "˜damage' to the genetic information. Not how you evolve new species"¦

It is a series of point mutations in a voltage-gated sodium channel, not a neurotransmitter The specific amino acids are listed in the Nature paper. There is no reduction in protein levels; the amino acid changes prevent tetrodotoxin from binding to and blocking the channel pore. Similar mutations occur in other tetrodotoxin resistant organisms. Some TTX-resistance mutations do make slight changes to channel kinetics, but the protein still functions as a sodium channel. Bear in mind that only some vertebrate sodium channels are TTX sensitive (e.g. skeletal muscle and some neuronal channels). Others are naturally TTX resistant (e.g. cardiac and some neuronal sodium channels). So you can only characterize TTX resistance as a "damage" to the genetic material if you have in mind some idealized sodium channel in an idealized environment. In the real world, everything is relative.

FWIW, the channel in question is the garter snake skeletal muscle sodium channel. If I wrote neuronal earlier I apologize — a slip based on the fact that both muscle and neurons contain TTX sensitive channels.

With regard to evolution of new species, speciation is related to changes in chromosome number, breeding behavior, etc — things that induce reproductive isolation. It is not directly linked to the evolution of new traits. However, once speciation has occurred, new traits that occur in one species cannot transfer to the other. Thus differences between the two species will accumulate. Since the discussion involved the effects of natural selection or random mutation within a population, your comment on speciation is something of a red herring.

Although the Nature paper that I originally referred to is only available with a subscription, several other papers seem to be available for free, and most of my comments are drawn from them. Check them out. There's some really cool data:

Fun fact: the authors include Edmund D Brodie, JR and Edmund D. Brodie III. A father and son science team!

http://www.bio.indiana.edu/~br...

http://www.harding.edu/USER/pl...

http://www.bio.indiana.edu/~br...