The Talk.Origins Archive Post of the Month: November 2008

Subject:    | Reasonable Guesses
Date:       | 25 Nov 2008
Message-ID: | d2824612-bfe6-4045-9dd8-7225233df02d@l39g2000yqn.googlegroups.com

Sean Pitman wrote:
>>>>> The question is, what are the odds that your stories are true? You
>>>>> don't know the answer to that question. You don't have the first
>>>>> clue. Why not? Because you don't subject them to any sort of
>>>>> statistical analysis. All you have is bald assertions and fantasy
>>>>> just-so stories. That's it.

Howard Hershey replied:
>>>> I have repeatedly pointed out that there are statistical methods
>>>> for identifying that something occurred in a manner consistent with
>>>> common descent. But I am not interested in producing GIGO^[1]
>>>> probabilities that have no relevance to *real* evolutionary
>>>> processes. I leave producing such bullshit nonsensical irrelevant
>>>> numerology to people like you.

Sean Pitman wrote:
>>> Common descent argument's are not the same as arguments for the
>>> mechanism of common descent.

Howard Hershey replied:
>> They certainly are relevant for identifying historical relationships.
>> Such historical relationships are necessary to identify those
>> features that were present in ancestral organisms that could be
>> *modified* to produce what exists in more modern organisms. Again,
>> pretending that one can generate probabilities based on the size of
>> the end system alone is pretending that evolution works like a fair
>> lottery rather than a historical process. Any calculation based on
>> that false assumption will NOT produce the "odds that *some* organism
>> could have generated feature x". It might produce the "average" odds
>> that a *randomly chosen* organism could evolve that feature. But
>> such odds effectively lump in all the organisms which have
>> essentially no chance of evolving x with any organism that has
>> features that can be modified easily to produce that feature.

Sean Pitman wrote:
> You have to have at least some idea of the likely existence of some
> creature with pre-existing features that are close enough to target
> "X" to find it in a reasonable amount of time using the mechanism of
> RM/NS^[1]. You have no idea as to the odds of such an existence
> whatsoever.

Howard Hershey replies:
Of course I do. I have evidence that motors that have sequence (and, more importantly, structure) similar to that of the motor in flagella, exist in cells in the absence of flagella. Indeed, similar motors also exist in cells with flagella, but do not interact with flagellar proteins. That is true both for the eubacterial flagella and the archae. Rotatable pores, of course, are a dime a dozen, since special effort has to go into making a non-rotatable pore.

That means that the probability of generating a pore with motorized rotation is *necessarily* smaller than any value calculated on the basis of the end size of the total system. Only one protein (the linker) needs to be formed. No other protein needs to change at all to change the system from one that lacks the *function* of motorized rotation to one that has that *function*. Yet the only calculation you make rests on the assumption that it is impossible to generate motorized rotation unless you do so by starting with a completely randomized system. In fact, I have suggested that the new *function* of motorized rotation can occur, at a minimum, in one mutational step by the formation of one of several possible chimeric linker proteins. I certainly don't claim that *every* pore and *every* motor that ever existed can form such a linker that provides the new *function* (why am I the only one of us who talks about gain, loss, modifiction, or emergent *function* rather than pretending that *size* is a substitute for *function*). One of the pores and one of the motors that *was* capable of doing this step was, not surprisingly, most likely closely related in sequence (actually structure) to the one that did.

I *also* don't necessarily claim that, in the original mutant that linked pore and motor to produce the *function* of motorized rotation, that, in the original, the *function* also included organismal motility by flagellar activity. [That was the way that, in the experimental model, the linkage was selected, but if one could identify linkage that had the *function* of motorized rotation but not organismal motility, that would have worked as well.] Once you have the *function* of motorized rotation, and there are certainly possible utilities for that function alone in some environments, gaining the emergent function of organismal motility has a clear quantitative pathway with potential selectively useful steps of increased rate of rotation along the way.

Do I *know* that this is the pathway taken? No. Of course not. But it hardly is an unlikely or impossible step between a specific state that can (and does) exist in cells and a modification that produces a new *function* of motorized rotation. It is, in fact, quite consistent with the subfunction of the 'pore' part of existing flagella and the subfunction of the 'motor' part. In fact, those functions do not need to change at all.

I do note that you claim that the *function* of toxin transport and the *function* of flagellar motorized rotation for the pore must be x number of proteins different. That is nonsense. Flagella themselves, particularly in bacteria that cause gastrotestinal infections, can transport secreted proteins important to toxicity as well as contribute to toxicity by the flagellin proteins acting as adhesion elements. [My personal opinion is that motorized rotation was *initially* a way of searching a larger amount of space per unit time of an adhesion system and that organismal movement was an emergent property.] Again, what you call *THE* function of flagella is merely one of the functions that is possible for the same structure.

> Your sequence data does give you this information. You simply
> make up the needed creature with a just-so story.

No. I pointed out the unambiguously present subfunctions of current flagella that could easily have independent utility to bacteria before the linkage event which added the *function* of motorized rotation. And pointed out that similar systems actually do exist in bacteria with similar structures and sequences. I also point out some of the *other* selectable functions that flagella have. The criteria is not the invention of just *any* starting point some arbitrary distance away. It is pointing out the *functional* criteria of potentially useful intermediate steps.

You yourself recognize that size, by itself, does not determine the size of the gap whenever you lie and say I can choose any starting point in total sequence space and then object when I do just that.

> You don't know if the creature exists or not. You just know it had to
> have existed because you are so sure RM/NS did the job.

No. I just know that your statistics are based on the bogus idea of random assembly from some average or arbitrarily large distance through some arbitrarily declared gap where the sequences have no function at all.

> Your problem is that you don't actually have any statistical analysis
> to back up the notion that your just-so story is remotely likely. Your
> simply assertion is all you really have - a fairy tale story. Not
> science.

My fairy tale story that these features evolved from similar structures by modification of those pre-existing structures has structure and sequence evidence to support it. New systems have traces of history that cannot be (statistically) simply a matter of chance. Your idea that these systems arise by complete chance assembly is the one that is based on false assumptions.

>> The *actual* odds of feature x evolving depends on the existence
>> (or not) of organisms of the last type, not on how many organisms
>> have no chance of generating that feature, no matter how useful.

> Again, the question concerns the odds of your needed organisms or
> biosystems existing. What are the odds that these needed creatures or
> systems ever existed in real life? You just don't know.

If there were no sequence or structure homologies among proteins and systems with modified, emergent, novel, or additional functions, I might not know whether there were creatures with the proper structures. But gene families are the rule rather than the exception. Gene families would not exist in your model of evolution where the only relevant factor is the end size.

> You simply argue that because they could have existed in the way you
> need them to have existed, that the odds that they did exist in this
> manner are "good".

And my idea is supported by actual evidence that the sorts of features (in a functional and structural sense) I require not only could exist, but do exist. And the mechanism of modification of pre-existing systems certainly does exist in nature. Your idea that proteins are essentially assembled by random assembly from something somewhere somehow is not supported. There is no mechanism for magical poofing or random assembly from some average or maximally distant sequence.

> Really now ... what is this notion actually based on? Have any
> statistical backing to support your assertion that the odds of such
> fortuitous organisms existing are actually good?

The statistics saying that genes that share function are related by descent and not by chance is quite strong. That also goes for genes in the same gene family.

>> Odds based on the assumption that all organisms are equally likely to
>> evolve feature x do NOT tell us anything about the odds of that
>> feature *actually* evolving *unless* you can demonstrate that all
>> organisms are *equally* far away from evolving that feature.

> The odds in question concern your notion that any organism is "likely"
> to exist in close proximity to a given potentially beneficial target
> or targets.

>> Which, of course, by positing the straw man "747 in a tornado" model,
>> you are assuming. But assuming that something is so is not what we
>> do in science. What we do is test our assumptions. What *evidence*
>> do you have that all organisms are *equally* far away from evolving
>> any feature? Is that equal probability a common feature of those
>> things we do see evolving?

> What a crock! You don't test your assumptions at all. Where is your
> statistical test for your notion that ANY organism is remotely likely
> to exist like you need it to exist?

All I have to do is show that the odds of that existing is much higher than the odds you propose. Again sequence evidence both within function and in related gene families say I am right and your idea that evolution works by random assembly from scratch is wrong.

Sean Pitman wrote:
>>> I'm not asking you to support the common descent theory
>>> here. I'm asking you to support the mechanism of RM/NS.

Howard Hershey replied:
>> Which part of the mechanism of RM/NS do you think does not exist in
>> nature? Do you think that mutation is not random? Do you think that
>> the rates of mutation are unmeasurable? What is your problem with the
>> concept of RM as the basic and ultimate cause of all natural 'genetic
>> variance' in populations?

>> If there is RM, then the question is whether NS occurs in nature.
>> From my perspective, the opposite of NS is not stasis (because
>> genetic stasis *requires* NS against change), it is non-selection.
>> The consequence of non-selection (which means that selection is
>> significantly indistinguishable from the effects of chance alone) is
>> neutral drift (change over time). Selection, positive or negative,
>> and the *strength* of that selection, is conditional on local
>> environmental conditions. Selection is measured by the metric of
>> relative reproductive success. Because *any* genetic variation must
>> exist somewhere on the line between absolute selection for and
>> absolute selection against (with selective neutrality being the area
>> near the midpoint) in a particular environment, all RMs are subject
>> to NS. Positive selection or neutral drift leads to changes in
>> genomes. Your ideas may differ. But you need to point where you
>> think there is a problem with the mechanism of RM/NS. Just saying
>> you're against the mechanism of RM/NS doesn't tell me much. I do
>> think that the *mechanism* of RM/NS occurring in nature is quite
>> strongly supported experimentally and by observation.

That is not what you said. What you said is the RM/NS cannot be supported as a valid mechanism of change. If you want to clarify, please do so. Don't laugh at me because you state things in a particularly obtuse and ignorant way.

> That's not the question. The question concerns the odds of your
> proposed starting point being remotely likely to actually exist in any
> real gene pool of options. Hello!

And what are the odds of your nonsense GIGO bogus numerology actually being anything like an honest description of the evolutionary process? Zero. Nil.

> Where have you been the last several years we've been debating this
> concept? Oh, I forget. You have the memory of a goldfish because of
> your whole "Hershey collective" thing ...

No. You have already conceded, in the past, that your "odds" are not the real odds of something *actually* evolving but represents, variously, minimum likely something or average gap size or something or something that you then discard and hand-wave a smaller number that you can pretend doesn't make you look completely foolish. What I am doing is using actual evidence, based on things that *actually* exist in *real* organisms to support a *possible* pathway and *specifically* identifying *specific* gaps and what sorts of mutations could cross those *specific* gaps to produce a new, additional, modified, or emergent functionality.

>> OTOH, retention of genetic traits that would otherwise be deleterious
>> to survival/reproductive success *almost always* (exceptions include
>> linkage to strongly selected genes and meiotic drive genes) requires
>> "intelligent design", aka "artificial selection". Usually these
>> otherwise deleterious traits have a benefit to the "designer" (aka,
>> humans). Examples include the domestic turkey, triploid seedless
>> watermelons, and toy poodles.

*All* selection is for function, specifically for the effect that functional difference has on relative reproductive success.

> No form of function-based selection (even if humans are involved) is
> going to get you a novel beneficial system beyond the 1000aa^[1] threshold
> this size of trillions of years of time.

> If you think otherwise, you must have some sort of statistical
> evidence to suggest why your fortuitous starting points are likely to
> have ever existed.

That would be moving the goal posts to a 'gap' further back in time. You are essentially asking how and why a pore could evolve without it being specifically for the production of a flagella and utterly useless until a flagella forms. Or what use is a motor unless it moved a flagella. The relevant point is that rotatable pores exist without being part of a flagella and so do motors without any teleologic necessity that they be capable of becoming part of a flagella. But the odds of flagella forming when such systems exist are clearly much, much, much, much greater than if only the end size were relevant and the flagella were the *only* possible function that could exist for the system (which is what your math proposes).

>>> The statistical methods you're describing here only demonstrate that
>>> certain degrees of similarities are more likely the result of some
>>> non-random mechanism.

>> The analyses show that the pattern is not *just* a 'non-random
>> mechanism'. These methods also can explicitly rule out the idea that
>> these patterns are the result of difference due to functional
>> necessity. The only natural (supernaturalism can do anything)
>> process that *is* consistent with these results is common historical
>> descent.

> Again, common descent theories have nothing to do with explaining the
> mechanism of RM/NS.

You again are pretending that your argument is against the *mechanism* of RM/NS. Yet you contradict yourself on that account by pointing out that you know that both RM and NS are known features of biology.

> That particular mechanism is what is under discussion here - not CD.
> Where are your statistics to explain how RM/NS work to find novel
> targets at various levels of functional complexity?

The *mechanism* of RM/NS is not any different at any level of functional complexity. What feature of the *mechanism* of RM/NS has to change if the protein or protein system is larger than if it is smaller?

Sean Pitman wrote:
>>> Beyond this, the mechanism of RM/NS is simply assumed to have been
>>> able to do the job. This particular assumption is what I'm
>>> questioning here.

Howard Hershey replied:
>> If RM in the *absence* of NS (neutral drift) can explain the observed
>> overall quantity of change given the available time (as it does for
>> humans and chimps), it is not an *assumption* that RM/NS *could* also
>> accomplish that. We know, from experiment and observation that
>> *when* selection is present, the amount of change (negative or
>> positive) is much more rapid than when there is no selection. Do you
>> have evidence that the mean or average amount of difference in chimp
>> and human genomes *cannot* be accounted for by drift alone?

>> Where they look for sequence regions that have changed more rapidly
>> between humans and chimps than between chimps and mice or rats. They
>> found about 200 such regions, with only 3 encoding proteins. Most
>> are undoubtedly regulatory. But mutations in regulatory regions are
>> often quantitative in their effects rather than qualitative.

>> Another difference is in copy number of particular genes. Some of
>> these may be particularly important for the differences between
>> humans and chimps.

>> But there is absolutely nothing that makes any of these differences
>> impossible by RM. All of the changes are the sort we see being
>> produced by various forms of RM today. And if they are being
>> produced, clearly NS is going to affect them (keeping in mind that
>> the absence of selection is on the scale of NS from positive through
>> neutral to negative).

> You love to go to the differences between humans and apes precisely
> because we do not yet know very much about the functional differences
> between these two kinds of creatures.

It doesn't matter what the functional differences are. The point remains that whatever they are (and they include difference in about every bone and in levels of abstract intelligence and hair and strength and a lot of other phenotypic differences) there is no evidence that it requires crossing your hypothetical gaps.

> Stick with what we do know more about Howard - like functionally
> beneficial sub-cellular systems. Try explaining how to get from a
> TTSS-like^[1] system to a flagellar motility system using RM/NS for
> example.

I have already pointed out that *flagella*, actual bacterial flagella, act as protein export devices for toxins. In addition to acting as adhesion systems and a number of other *functions*. You seem to be stuck on the idea that "flagella" is a teleologic goal function and cannot be composed of subfunctions or have additional functions. You are wrong. That is, flagella *are* a TTSS-like system. All eubacterial (but not arcaeal) flagella export flagellins. Some export other proteins. That is, some have *both* functions and the *gap* between the two *functional* states is zero.

> Use real statistical odds estimates to support the likelihood that
> your needed steppingstones will actually exist.

>>> Where is the statistical analysis supporting this particular
>>> mechanism? There are many statistical papers published on the
>>> concept of common descent. There isn't a single one that I know of
>>> published on the mechanism of RM/NS.

>> Sure there are. What they all say is that the strength and direction
>> of NS is a function of the local environment. There are also lots of
>> studies that show that mutation is random. What sort of statistic are
>> you looking for?

> We all know that the strength and direction of NS is a function of
> local environment. The question here concerns the evolution of novel
> functional systems that were not in the gene pool before.

Change in *function* simply doesn't always require a large change in *structures* or *sequences*. *Function* is NOT structure and sequence. It is related. But there is no one to one correspondence.

> You argue that such evolution depends upon the starting point. Again,
> what are the odds that your needed starting point will actually exist?

What are the odds that cells can have rotatable pores and motors without having flagellar functions? Ans: one. We know that such structures and functional systems exist in cells. Now, how many of those can be modified to link together and generate the new added *function* of motorized rotation. That I cannot say. But it clearly is much more probable than the idea that flagella starts by random assembly from scratch in a way where the end size would matter.

> You conjure up all kinds of starting points when you need them without
> ever considering the odds that your conjurings are remotely likely ...
> That's not science.

Let's see. I *specify* a *specific* gap between *actual* functional states. Show that the starting *functional states* can actually exist. And point out an *actual* gap size that can cross that *specific* gap. You generate an arbitrary size. Ignore how many gaps are needed. Never discuss any *specific* gap. Generate an odds that invokes a bogus straw man model of evolution. Then try to hand wave a smaller number because you recognize that your number isn't about any *specific* real gap. And you call what *I* do conjuring?

>>> All scientific papers simply assume that RM/NS did the job without
>>> actually subjecting this assumption to real scientific
>>> investigation. There are no papers, not a single one, dealing with
>>> the odds that the proposed mechanism of RM/NS actually did the job.

>> RM/NS doesn't have a "job" to do. That would be teleological
>> thinking that assumes that the mechanism is goal-directed.

> Wrong. RM/NS does have a job to do - to find novel beneficial
> targets. That's the job of this mechanism. Without this job actually
> happening, evolution wouldn't happen.

>> Both RM and NS happen as a consequence of the nature of our genetic
>> systems and the fact that organisms interact with their local
>> environments.

You are the one claiming that there is something 'wrong' about the mechanism of RM and NS that is somehow related to the size of the system the mechanism is working on.

> We are talking about novel beneficial targets being found. What are
> the odds of a novel beneficial target being found by RM/NS?

Depends on the starting points. If you have a *specific* gap between *specific* functions that cannot be crossed because all the *possible* intermediate pathways between these functional states are too long, why don't you show *that* as your example. I have given an example of a *specific* gap and the functions and structures of both start and end. Where are your *specific* gaps where you state what the starting point is and what the end point is?

> In short, what are the odds that a starting and target point will
> actually be close enough together for RM/NS to find it in a given
> period of time?

In some cases, quite good. In others, quite bad. But not because of the size of the end result. Again, evolution is not a fair lottery where all organisms have the same chance of "winning".

[1] Acronyms:
NS: Natural Selection
RM: Random Mutation
GIGO: Garbage In Garbage Out
aa: amino acid (protein building block)
TTSS: Type-III secretory system (a needle-like structure that some bacteria use to inject toxins into other cells)

Does Natural Selection give every individual an equal fair chance at a beneficial mutation?

Post of the Month: November 2008

Does Natural Selection give every individual an
equal fair chance at a beneficial mutation?