Re: Direct Experimental Evidence for Non-Beneficial Gaps

Seanpit wrote:
On Jul 9, 9:34 pm, John Harshman <jharshman.diespam...@xxxxxxxxxxx>
wrote:

[snipping parts that require me to have read things I still haven't got to]

You have to explain evolution from the perspective of a particular
gene pool that has its own particular functional constraints.
No you don't. That assumes that the protein in question is the only
thing that's allowed to have evolved. And when you're talking about
probabilities you have to consider all the possible events that didn't
happen as well as the ones that did.

The protein in question is pretty much the only thing that is allowed
to have evolved to fill the particular niche that it fills -
especially when you're talking about a function as restrained as the
CytoC protein.

You misunderstand the point. I'm talking about other proteins in the system also being allowed to evolve, specifically cytochrome b, c1, and the various pieces of cytochrome oxidase.

Exactly. That means you *are* talking about non-beneficial gaps. You
are basically saying that they don't exist. That each mutational step
can be functionally advantageous. That's wrong. Each mutational step
cannot be functionally advantageous since the minimum structural
threshold requirements for the systems in question are simply too high
beyond a few hundred fairly specified amino acid residue positions.
This is the claim. I don't believe it. How about starting with a gene
family?

What do you mean by "gene family"? You mean a single gene that codes
for a single protein? Pick any one you want. Most are well below the
1000aa threshold as single gene families. Most functional systems
that go beyond the 1000aa threshold minimum are multi-protein systems
that are coded for by multiple "genes".

Are you telling me you don't know what "gene family" means? That seems odd. A gene family is composed of multiple homologous genes in a single genome; paralogs, that is, that presumably originated as duplications. These are the most obvious examples of systems that I would claim would have evolved divergently, starting from identical sequences. It seems an obvious place to look for a test of your ideas.

Now the problem here is your idea that "kinds" were separately created, and thus that gene families were also created separately in each kind, and thus that the members of the family are not homologous. We might get around that if we knew what a "kind" was, because there might have been enough duplication and divergence within a "kind" to allow for some test. Could you explain what a "kind" is, and how to recognize one?

You simply cannot build up an interactive system beyond this level of
complexity because of the linearly expanding non-beneficial gap
problem.
Are you saying
such divergence isn't possible,
It is possible. It does happen - all the time. It just doesn't happen
beyond very low levels of functional complexity.
or are you saying it can't go very far?
That's right . . .
Can you, for example, name a single protein family that encompasses
different "novel" functions such that it would be vanishingly unlikely
to have evolved by known mechanisms?
I can name you several protein-based systems that are overwhelmingly
isolated since they all require well over 1000 amino acid residues all
working together at the same time in a specific orientation with each
other: DNA transcription, RNA translation, vesicle transport, ATPase,
pinocytosis, exocytosis, flagellar motility, amoeboid motility, etc.
Not to mention organoid systems like mitochondria, Golgi bodies,
centromeres, etc.
You persist in answering all the questions you wish I had asked rather
than the questions I actually did ask. I'm talking about gene/protein
families. Do you know what those are?

Do you not understand that multi-protein systems also qualify? It is
rather difficult to find a single-protein system that has a minimum
structural threshold beyond the 1000aa or 1000-codon limit.

Doesn't matter, if different members of a family are part of different systems. Anyway, it's a way to sneak up on the question.

Now mitochondria, since you mentioned them, present a special problem
for separate creation, since they are obviously bacterial endosymbionts,
and endosymbionts with a single point of insertion into the eukaryote
tree. Do you really want to diiscuss mitochondria?

The whole endosymbiosis theory for mitochondria is a separate issue;
one I do not care to get into with you at this point. The question at
hand is, can you find any system close enough to a system like ATPase
to have evolved it via the mechanism of random mutation/natural
selection (RM/NS) this side of trillions of years of time?

That's what I'm trying to deal with using the idea of gene families.

I'm not asking for the re-evolution of the bacterial flagellum from
scratch. I'm asking for a demonstration of just one of the proposed
steps in the flagellar evolutionary model - or any other demonstration
of the evolution of any other novel functional system with a minimum
structural threshold of more than the relatively paltry 1000aa. This
shouldn't be so hard. After all, such demonstrations at the level of
a few hundred residues are very easy to come up with. Why is the
1000aa level so difficult to demonstrate? Hmmmm?
Largely because nobody knows what you're talking about when you repeat
that mantra. I'm trying to sneak up on it with my question about gene
families.

I've explained the multi-protein concept many times in this forum
already. I really don't understand what you don't understand about
the 1000aa threshold level of complexity?

You're talking about a system in which at least 1000 residues are not free to vary without making the entire system nonfunctional? Do you have any evidence for the existence of such a system, or that anything you have mentioned is such a system?

You call such scenarios "plausible"? - when every single one of their
proposed steps involve vast gaps in non-beneficial genetic changes?
How can you say that? It involves only random phenotypic variance of
exactly the sort that regularly exists in living populations. It assumes
only that this random variance will be recharged by mutation, which
seems a reasonable assumption not requiring descent into any genetic
details.
We aren't talking about the evolution of eye color here. We are
talking about unique functional aspects between different kinds of
eyes. These differences are not simple phenotypic variances.
Yes they are. That's the point of the Nilsson & Pelger paper. Each
single step is within the range of random phenotypic variation in living
species.

Not true. Not if you actually look at the functional genetic changes
that are required.

How can you know this? Have you actually looked at the functional genetic changes that are required?

If you think otherwise, please do quote the
specific part of the paper that details the required functionally
relevant genetic changes to get from one type of eye to another. That
information simply isn't there in the Nilsson & Pelger paper.

That's true. They don't consider genetics. They assume that enough genetic variation will happen to keep random phenotypic variance in the population.

In their models (models which are not even based on computer
simulation by the way - contrary to the claims of those like Richard
Dawkins in his description of the paper), Nilsson and Pelger made no
attempt to simulate the internal workings of cells.

This is true. The models are not based on computer simulation. They're exactly calculated. But I don't see why that would be a defect. Nor do I see why they would have to simulate the internal workings of cells.

They worked at
the level of tissues: the level of stuff made of cells rather than the
level of individual cells. Nilsson and Pelger began with a flat retina
atop a flat pigment layer and surmounted by a flat, protective
transparent layer. The transparent layer was allowed to undergo
localised random mutations of its refractive index. They then let the
model deform itself at random, constrained only by the requirement
that any change must be small and must be an improvement on what went
before.

All true.

The problem with this whole senario is that it does not evaluate the
necessary underlying genetic changes at all needed to get from the
starting point of a light-sensitive spot to a camra-like human-type
eye. It is entirely based on seemingly small morphologic changes.
Getting from a single celled system to a multi-celled system and then
getting all the individual cells to work together to warp into a new
structure over generations is not nearly as simple informationally
speaking as the morphologic steps would have you believe. Not even
close.

Getting from a single cell to a multicellular organism is not at issue in eye development. We start with a bilaterian animal. And a bilaterian also starts with a developmental tool kit that tells cells how to work together. You're making difficulties that don't exist.

The 1-percent steps they claim to have made: in what units are they
expressed? And how much biological change is represented by each step?
Nilsson and Pelger do not say.

I don't remember, and I can't currently lay my hands on my copy. Though percent is usually not expressed in units; it's a dimensionless ratio.

Nor do they coordinate morphological
change, which they treat as simple, with biochemical change, which in
the case of light sensitivity is known to be monstrously complex.

Light sensitivity is assumed to be present initially, so this is irrelevant.

Does invagination represent a process in which the patch changes as a
whole, like a balloon being dimpled, or is it the result of various
local processes going off independently as light-sensitive cells
jostle with one another and change their position? Are the original
light-sensitive cells the complete package, or are new light-sensitive
cells added to the ensemble as time proceeds? Do some cells lose their
sensitivity and get out of the light-sensing business altogether? We
do not know, because Nilsson and Pelger do not say.

Nor do they chart the courses of individual atoms, or explain what the various organisms had for dinner.

Getting
such a functional variance when it did not already exist requires the
crossing of a huge non-beneficial genetic gap that cannot be traversed
by any series of shortly spaced sequentially beneficial mutational
steps.
How can you assert this? There is in fact a simple genetic mechanism
that could create the sort of needed distribution of variations, which
would be slight changes in the transcription factor binding sites of the
genes involved that would make them just a little bit more or less
sensitive. Standard evo-devo. This would seem to be within the realm of
your "few hundred" residues, since binding sites are only a few tens of
bases long at most. So I don't see how even you can complain.

And you think increasing or decreasing proteins that are already being
produced is going to be enough to change one type of vision system
into another? Think again . . . You simply cannot turn an light
sensitive spot into a human-level vision system via such a mechanism.

And you know this...how? I repeat the observation that most differences in animal morphology do not reflect the evolution of new and different proteins, just different expression patterns of those proteins. Further, when new proteins are involved, they generally arise through duplication and differentiation of existing proteins. This is commonly known in evo-devo.

Sure, the morphology doesn't seem like much between these proposed
evolutionary steps, but the underlying genetic changes needed are
absolutely enormous.
What is your evidence or argument for this claim?
This is true for just-so stories of eye
evolution as they are for flagellar evolution - like the best one I
could find proposed by Matzke. How are such scenarios statistically
"plausible"? They simply aren't. Not remotely so.
Why?
I ask you the same question. Please list out just one of the steps
that you think is phenotypically so simple and then demonstrate that
the underlying genetic differences that would be required are small
enough to cross in a few hundred million years via random mutation
alone.
Dude, we're talking about something that a single point mutation could
handle, and we're talking about the degree of variation that's seen
within populations today. How can you say that current within-population
variation is an unbridgeable gap?

Dude, you're wrong. There is no way any series of sequentially
beneficial single point mutations could do what you claim they can.
Absolutely none. You have no idea how complex the required underlying
genetic changes must be to get from one step to the next in the
proposed pathways of eye evolution.

Do you? How do you know? You continually confuse the claim that I can't show something to be true with the claim that you can show it to be untrue.

If you think otherwise, then by
all means, present your *genetic* step-by-step evidence where 1,829
steps proposed could go from a light-sensitive spot to a camra-like
eye via a series of sequentially beneficial single point mutations.
That's absolute nonsense.

Why? Do you deny that there is random genetic variance in populations of the magnitude needed to produce observed phenotypic variance? Do you deny that there is enough observed phenotypic variance? Do you deny that phenotypic/genetic variance can recharge after selection moves the mean? Do you deny that point mutations in promoters can produce new binding sites, eliminate old ones, and render current ones more or less sensitive? Do you deny that these changes can produce small variations in phenotype of the sort needed? Otherwise, this is just another "god of the gaps" argument of the sort that requires a movie of a land animal morphing into a whale in order to believe that it happened.


I see evidence that it can move a character
indefinitely far from the original population mean, given the right set
of changes in environment.
The odds of success by random mutations, small or large, are exactly
the same. The odds that a change in environment will cause the
realization of a beneficial target are also exactly the same as a
random genetic mutation.
Can you explain that assertion?

I meant the second assertion: the odds that a change in environment will cause etc.

As I've pointed out many times,
common descent is evolution, even if God personally zaps every
mutation into being, or zaps multiple mutations at one time to
cross your "neutral gaps".

That's not evolution in the Darwinian sense of the term. That's slow
creation.

> That's a very unusual definition of "evolution". It seems to fit more
> with the definition of "slow creation" than with what any mainstream
> scientist would call "evolution". Really, such slow creation is not
> evolution at all in any standard Darwinian-style sense of the word.

Call it what you like. I would call it theistic evolution, which is a
term invented long ago for just such notions. My main object here is to
determine why you reject that option. So far I have no idea other than
that it doesn't fit your conception of Genesis.

As I've told you before, I'm not interested in going on and on with
you about your ideas of common descent at this point. I've already
been around and around with you on that. You're idea regarding common
descent simply aren't convincing to me.

I'm not asking you to argue about my ideas on common descent. I'm asking you to justify your claim to know that "slow creation" can be rejected as a viable hypothesis.

.

Relevant Pages

  • Re: Can any old earther refute common genetic ancestry?
    ... And mutations include point substitutions, ... As there are billions of such observations this is powerful support for the factuality of common descent with modification through the agency of natural science and other processes. ... The same holds for DNA sequences of homologous genes, or for the gene contents of organisms. ... In the past genetics assumed that a gene expressed for single well defined trait or function. ...
    (talk.origins)
  • Re: Can any old earther refute common genetic ancestry?
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    (talk.origins)
  • Re: Direct Experimental Evidence for Non-Beneficial Gaps
    ... gene pool that has its own particular functional constraints. ... I'm talking about other proteins in the ... relevant genetic changes to get from one type of eye to another. ... They don't consider genetics. ...
    (talk.origins)
  • Re: Direct Experimental Evidence for Non-Beneficial Gaps
    ... gene pool that has its own particular functional constraints. ... I'm talking about other proteins in the ... They don't consider genetics. ... see why they would have to simulate the internal workings of cells. ...
    (talk.origins)
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