Re: Evolution increases the computational ability of organisms.

Tim Tyler wrote:

John Harshman wrote:
> Tim Tyler wrote:
>> John Harshman wrote:
>>> Tim Tyler wrote:
>>>> John Harshman wrote:
>>>>> Tim Tyler wrote:
>>>>>> John Harshman wrote:
>>>>>>> Tim Tyler wrote:

>>>>>>>> I have said what I mean quite a few times now. I think evolution
>>>>>>>> is progressive in more than the Gouldian random walk way. [...]
>>>>>>>> Dawkins I attribute this to two main factors.
>>>>>>>>
>>>>>>>> One is "technological" progress: the cumulative "inventions" by
>>>>>>>> organisms of survival tech: photosynthesis, DNA, etc, favoured by
>>>>>>>> natural selection.
>>>>>>>>
>>>>>>>> The other is sexual selection, which tends to drive lineages in
>>>>>>>> arbitraryish directions, so many of their traits do not diffuse,
>>>>>>>> but rather are driven about.
>>>>>>> But they are driven in arbitrary directions. Again, nobody is
saying
>>>>>>> that the mechanism of all evolution is drift, just that
environments
>>>>>>> vary in unpredictable ways so that a course driven by selection
alone
>>>>>>> can act quite like a random walk.
>>>>>> Well, I won't argue with that - except to say that it was not
>>>>>> Gould's point. Gould argued for neutrality in a *particular*
>>>>>> case.
>>>>> What particular case are you talking about here?
>>>> The one in Life's Grandeur/FH - the idea that complexity
>>>> is a neutral trait overall.
>>> I don't have the book in front of me. Is he really arguing that it's
>>> neutral, or that different degrees of it are advantageous in different
>>> environments? "Neutral" is a highly specific term in biology.
>>
>> Fluctuating selection would satisfy Gould equally well.
>>
>> "The modal bacter: Why progress does not characterize the history of
>> life"... is his chapter title and theme.
>>
>> Probably the major theme is that complexity follows a random walk
>> bounded at the low end by a wall - and that this mechanism explains the
>> origin of complex organisms - without invoking any kind of selective
>> mechanism favouring progress.
>
> So...I'm vindicated here?

You are making a similar argument to Gould.
Both you and he are emphasising overall neutrality.

No we're not. Please don't use "neutrality", which is a technical term
in biology. So we are agreed that your claim "it was not Gould's point"
is wrong?

>>>>>>> Most "technological progress" is a local adaptation to some
environment.
>>>>>>> If the environment changes, technological progress can involve
reversal
>>>>>>> of the previous progress, and that doesn't sound like progress
to me.
>>>>>>> Some adaptations are useful in a wide variety of environments,
and so
>>>>>>> are unlikely to be lost in most events. These are quite rare [...]
>>>>>> Pah!
>>>>>>
>>>>>> DNA? RNA? Enzymes? Proteins? Sex? Lipid cell walls? Cellulose?
>>>>>>
>>>>>>> I don't think they justify a claim that evolution is in general
>>>>>> progressive.
>>>>>>
>>>>>> Your view that the accumulation of technology like DNA, RNA,
enzymes,
>>>>>> proteins, sex, photosynthesis etc does not make evolution
progressive
>>>>>> is duly noted.
>>>>> What exactly does "progressive" mean here, and why should 6
events in 4
>>>>> billion years be considered the norm?
>>>> Roughly, progress is intended as a measure of evolutionary competence;
>>>> of the ability to extract resources from an environment before
>>>> competitors do - and so on. It is related to fitness.
>>>>
>>>> It is not just represented by 6 events - those were examples.
>>> How many events would you suppose?
>> Billions? I really don't know in much detail. Bacteria have
>> made an *awful* lot of useful biochemical inventions, and humans
>> have made one or two of their own discoveries by now.
>
> Please leave human technology out of this. Now it looks as if nearly all
> major bacterial inventions were finished a billion years ago or more,
> since the trees of the major metabolic guilds go that deep. And there
> are no more than a couple of dozen of those, however you slice it. I
> don't know how you're going to come up with billions, and I don't know
> how you will get a rate of progress out of it unless that rate is
> slowing down.

Each enzyme counts as a bio-invention - though some of
them will be dupes of each other.

And most of them will be slight variants of others. You can inflate the
number of inventions by counting each variant as a new invention if you
like. But that seems to devalue the concept.

>>>>>>>>>> It happens because ploidity-increasing events followed by
divergence
>>>>>>>>>> which is then reinforced by selection are relatively common
among
>>>>>>>>>> some lineages - while selection in the opposite direction is
>>>>>>>>>> obviously rather weak.
>>>>>>>>> This is confused. Are you saying that gene number generally
increases in
>>>>>>>>> evolution?
>>>>>>>>> I see no sign of that.
>>>>>>>> ?!? Have you looked?
>>>>>>> Yes, to the extent possible. What sort of evidence would you
like to
>>>>>>> present for your claim?
>>>>>> Ploidy-increasing events are rather common, as can be seen by
>>>>>> all the high-ploidy organisms out there.
>>>>> Not sure what you mean. Most organisms are either haploid or diploid.
>>>>> Polyploids are transient, because homologous chromosomes
differentiate.

[snip Paleopolyploidy]

>> I think my most sensible response at this point is: it
>> doesn't make much difference if the organism is classified
>> as polyploid or not - the point is that its genome has
>> been duplicated, and is larger than it once was.
>
> True, for a while. Note that genes are rapidly lost from the duplicated
> genomes, until we're back where we started.

Right, but selection gets a look in in the process -
if a duplicated section subsequently diverges into
something that's actually useful.

You were trying to justify a claim that genome length increases through
time, so your "but" is irrelevant here.

>>>>>> And we know selection
>>>>>> against junk DNA is remarkably weak - because related organisms with
>>>>>> lots of it do not appear to suffer in competition with those with
>>>>>> little - and because there is so much of it in so many non-bacteria.
>>>>> I would say that's evidence that it's either weak, or fluctuating, or
>>>>> both. But the fact that genome size fluctuates so much doesn't
suggest a
>>>>> consistent trend toward increase.
>>>> The bit of genomes which is junk is rather likely to fluctuate.
>>> Here we come again to the ambiguity you refuse to resolve, whether
we're
>>> talking about number of genes, size of the functional genome, or
size of
>>> the genome in general.
>> Again? Refuse? You specified the topic here in the section quoted
>> above. You said "genome size". I haven't attempted to switch the
>> context since then.
>
> Yes you have, right here. You try to dismiss fluctuating genome size by
> saying that's just the junk that fluctuates. This would imply that the
> size of the non-junk portion of the genome is what you are really
> concerned with. Or did you misspeak?

Put it this way: I'm prepared to put up with noise in the
signal, in order to get at least some signal. The noise is
not terribly interesting, but attempting to get rid of it
before measuring the signal would be a significant PITA.

That's not a response. It would in fact appear that the signal you are
talking about right now (genome size) is pretty much all noise.

>>>>>>>>> All you're doing is stating a mechanism that increases number and
>>>>>>>>> denying that any mechanism decreases number.
>>>>>>>> No: I'm suggesting the increase mechanism is powerful,
>>>>>>>> while the decrease mechanism is weak. This is true in
>>>>>>>> plants, and false in bacteria - but the plants are enough
>>>>>>>> to boost up the averages, so there is a net increase overall.
>>>>>>> Ah, so this supposed progressive mechanism is limited to plants.
>>>>>> No. It is /commonest/ in plants, though.
>>>>> So, if you were right, wouldn't plants consistently have larger
genomess
>>>>> than other groups?
>>>> Yes - if that were the main mechanism responsible for size increases.
>>> So we have come down to the notion that your proposed mechanism is at
>>> most a side issue.
>> My using the term "polyploidity" selected too narrow a target.
>>
>> There are many ways of duplicating genes and then the copies
>> diverging and adopting independent functional roles that do
>> not qualify as polyploidity.
>>
>> Another potential target for selection for large genome
>> size is mobile genetic elements. These typically benefit
>> from being as numerous as possible, and the bigger genomes
>> are, the more copies they can contain.
>
> Here I think there's a confusion of level and direction of causation.
> Mobile elements don't benefit from being numerous. It's just that those
> that replicate fastest increase in frequency in the genome.

I was asserting that mobile genetic elements *do* benefit
from being numerous. The more of them there are, the
more chances of them being copied around. They are just
like every other kind of gene in that respect.

I have no idea what you are trying to say there.

> But this is not selection on the genome, it's selection (of a sort)
> on the mobile elements themselves.

Yes, exactly.

>>>> I seem to recall previously defining genome complexity for you:
>>>>
>>>> The Kolmogorov complexity of the information in the genome -
considered
>>>> in base 4. Would you like me to specify the associated language?
>>> Ah, so this is the minimum length of an algorithm that would reproduce
>>> the sequence of a genome, yes?
>> Yes.
>>
>>> But wouldn't a completely random genome then be the most complex?
>> Yes.
>>
>>> In which case, you are claiming that the randomness of genomes is
>>> increasing over time?
>> More their length.
>
> If so, shouldn't your measure be genome length, not complexity? The
> simplest way to increase complexity is to increase randomness, not
length.

Genome length is another possible metric. It's associated with
genome complexity - because some of the genome is pretty mutated
and random. However, I had better not start discussing
genome length, or you'll be onto me again for goalpost moving.

How 'bout if I get onto you for having no clear idea what you're trying
to do or say?

>>> Now of course complexity would increase over time if length
>>> increased over time, but only if the increases in length were
>>> random additions of sequence.
>> No, the sequences just have to have a somewhat unpredictable
>> element. Mutations and redundancy in the genetic code make
>> this likely to be true after a while.
>
> Surely you're not supposing that the genetic code has much influence on
> genome randomness, given that such a small percentage of the typical
> genome is coding sequence. You need to think this through a bit more.

Obviously, redundancy in the genetic code only affects coding
sequences. My point was that, as *well* as a lot of the junk
getting mutated, even the selectively maintained coding regions
will be affected by mutational randomness.

If that was your point, what was the point of your point?

>>> Tetraploidization would in fact be only a minimal (a few bytes)
increase in complexity,
>>> the addition only of "do this twice" to the previous algorithm. So it's
>>> puzzling that you would give it such importance.
>> Consider the effect of subsequent mutations.
>
> One major effect would be to reduce genome size again. Now it might be
> that point mutations would increase complexity faster than deletions
> would reduce it, but I don't see how you can be confident in your
assertion.

After a genome duplication, you're unlikely to get back to the
complexity you started with unless you have something closely
equivalent to a genome halving.

True. What makes you think you wouldn't?

The original idea was that duplication is sometimes
followed by divergence and selection for the new function.

Some think this is how much constructive evolution occurs -
by duplication and divergence.

And I agree, depending on what you mean by "constructive evolution". Now
of course most of this is not whole-genome duplication, but duplication
of small regions. I don't see it as promoting a general increase in
either genome size or complexity, though.

>>> This also has nothing to do with function of the genome, which
seems odd.
>> Kolmogorov complexity is the most standard metric I can think of -
>> though it is hard to compute if you use a proper programming
>> language, rather than, say, a compressor.
>>
>> Getting into what part of the genome is functional and what
>> isn't soon turns into a rat's nest of ambiguity. I like
>> metrics that are a function of the genome only. It keeps
>> everything neat and digital.
>
> But is it meaningful? Your proposed measure doesn't seem to have
> anything to do with biology.

It's pretty similar to measuring genome sizes.

In the context we are discussing it in a big problem
with it is that it is hard to detect in the fossil
record.

None of which is a response.

>>> ...and deletion?
>> Deletions happen. I am not sure what you are asking here.
>
> Just checking. Would you agree that deletions too are more important
> than polyploidization?

IIRC, the most common indels are just inserting or
deleting a base pair or so.

True. The distribution of indel sizes is highly skewed. What's your
point, if any?

>>>>>> ...and there are those cases where the sheer quantity of DNA
>>>>>> is actually selected, e.g. because it influences cell size.
>>>>> Maybe. However, if that's true, then the optimum cell size, and thus
>>>>> genome size, can fluctuate over time, and we're back to the
random walk.
>>>> .../assuming/ that optimum cell size fluctuates randomly, that is.
>>> Do you see a reason why it wouldn't? It would be like the size of
>>> anything else. There is no universally optimum size.
>> Say Cavalier-Smith is right on:
>>
>> Nuclear volume control by nucleoskeletal DNA, selection for cell volume
>> and cell growth rate, and the solution of the DNA C-value paradox
>> http://jcs.biologists.org/cgi/content/abstract/34/1/247
>>
>> ...and genome sizes influence growth rates, and K-selected and
>> r-selected organisms make use of this by having large or small
>> genomes respectively.
>>
>> This wouldn't lead to a trend favoring large size - but it
>> would make a mess of the hypothesis that the distribution
>> of genome sizes is predictable from a random walk bounded
>> by a wall. There would be many abnormally small genomes,
>> from the r-selected organisms and many abnormally large
>> genomes, from the K-selected ones. You would have to
>> invoke selection to explain the results.
>
> I don't see this. In the real biota we see no separate clump of
> "k-selected" vs. "r-selected" species, but a continuum along which
> species are arranged between extremes. Presumably cell/genome size
> distributions caused by k vs. r selection would follow the k/r
> distribution too and would be scattered across the continuum. And as
> environments changed over time, the degree of k and r selection in a
> lineage would be expected to change too.

K vs. r selection may be a continuum - but species are not
evenly spread along it. I know of no K-clumping yet - but
there looks like there is a pretty huge r-selected clump of
species down around the single-celled organisms. Vast
numbers of these are opportunists who have little or no
parental care, and just try to turn their resources into
descendants as fast as they can.

Nobody says that a continuum has to be a uniform distribution. Now I'm
sure that most bacteria are indeed heavily selected for efficiency of
replication. But your original point seems to have tacitly disappeared. Yes?

I've discussed these myself - we know empirically
that many of these have relatively small genomes,
and that they are kept trimmed down by selection -
Cavalier-Smith's theory or no.

>>> But if in fact there is a drive to increase genome size (a goalpost
move
>> >from Kolmogorov complexity too, by the way), then it doesn't matter
what
>>> the size of the ancestral genome is. Size would only increase from
>>> whatever starting point there was.
>> Say there is some optimal genome size for that type of
>> creature, though? If the ancestral cell is below this,
>> there will be a progressive increase as time passes.
>> If the ancestral cell is above it there will be a
>> decline. The size of the ancestral cell might really
>> affect the result of the question of whether there
>> is progress or not - so sampling errors in its selection
>> are a real concern.
>
> Not at all. You were supposedly talking about the ancestor of all
> eukaryotes, so "that type of creature" is not really a meaningful term.

In that case it would refer to eukaryotes.

So "that type of creature" refers to all organisms under discussion? It
would seem to be a meaningless term, then.

> If there is an optimum size for any particular situation, and situations
> fluctuate, there's your random walk again. If instead, as you have
> proposed, there is a general pressure for increase, it doesn't matter
> where we start. If there is in fact a universal limit, then it depends
> on how close to that limit we started and how fast increase happens.
> But again the huge differences in genome size among species suggest that
> limit is either not particularly universal or extremely huge. At any
> rate, it seems to have no obvious influence.

Sampling error on the ancestor even changes the chances of
observing progress in the "random walk" theory. An ancestor
near the wall is more likely to have descendants further away
from the wall than one far from it is.

True if you consider only a single descendant. But we're talking here
about a branching process with many lineages, and in that case, the
ancestor farther from the wall will have its average descendant farther
from the wall than will an ancestor close to the wall.

That was my point: the "has there been progress in individual
eucaryote lineages since their LCA" question is somewhat
confounded by sampling error on the ancestor.

And my point is that it isn't; only your confusion makes it so.

I would say that eucaryotes have *diversified* since the LCA,
and have progressed as a group compared with it - since they
now live in a huge, diverse array of environments, instead of
just one, and are solving millions of different environmental
challenges - instead of just those facing one species.

Ah, so now progress equals diversification. Can't we settle on a
definition of progress? Here you have a definition clearly compatible
with diffusion.

>>>> If you ask: "has a lineage progressed since a particular ancestral
>>>> cell", the answer may depend a lot on what the properties of that
>>>> particular ancestral cell happened to be - and as one individual, its
>>>> measurements may be subject to considerable sampling error effects.
>>> Perhaps. And that's why it's a good reason to look at the whole
tree and
>>> ask whether whatever property you think is increasing really is
>>> increasing on most branches of the tree.
>> The problem I see with that is that inventions can be made - and
>> complexity can increase, by other mechanisms - in particular
>> by an increase in the number of branches.
>
> This is the advantage of reductionism: we can check one proposed
> mechanism at a time. Now if you want to modify your claims to be that
> genome size is not increasing but numbers of species are, we can discuss
> that too. But it will be a different discussion.

It sounds like I had best avoid that. It sounds like
goalpost moving to me.

Much too late for you to avoid goalpost moving. You don't appear to be
capable of focusing on a single topic at a time, or of remembering what
the topic was.

>>> If at any given time it's not especially mor likely
>>> to go up than to go down, regardless of where we
>>> started from, your theory is in trouble.
>> Not if the number of branches is increasing. That
>> might still represent progressive development.
>
> An odd definition of progress, but never mind. Since you are defining
> complexity roughly as genome size * number of genomes, sure, either
> factor could make the product increase. But we can consider them
> separately, as indeed seems wise. So if we've disposed of genome size
> increase, we can consider increase in species numbers. In fact we
> already have, in other posts. I don't see evidence for that either.

I think I shall stop reminding you than even Gould
agrees that species have increased in number and
that genomes have grown bigger. It is becoming so
tedious - and I know what you meant to say.

I doubt you do. I also doubt you know what Gould agrees.

>>>>>>> Genome size seems pretty randomly distributed over the tree of
eukaryotes.
>>>>>>> Would you consider that at all suggestive?
>>>>>> I would consider it to be totally inaccurate:
>>>>>>
>>>>>> Taxon #Records / No. of species
>>>>>> (%) Genome size range (pg) Mean genome
size (pg)
>>>>>> Vertebrates
>>>>>> Jawless fishes 26 17 (16) 1.3–4.6 2.3
>>>>>> Cartilaginous fishes 183 130 (13) 2.5–17.1 5.7
>>>>>> Lungfishes 14 4 (66) 50–133 90.4
>>>>>> Chondrostean fishes 38 22 (42) 1.2–7.3 3.5
>>>>>> Teleost fishes 1761 1354 (5) 0.4–4.4 1.2
>>>>>> Amphibians 870 463 (9) 0.95–120.1 16.7
>>>>>> Reptiles 406 309 (4) 1.1–5.4 2.3
>>>>>> Birds 274 205 (2) 1.0–2.2 1.5
>>>>>> Mammals 600 432 (9) 1.7–8.4 3.5
>>>>>>
>>>>>> "Eukaryotic genome size databases"
>>>>>> http://nar.oxfordjournals.org/cgi/screenpdf/35/suppl_1/D332.pdf
>>>>>>
>>>>>> There is massive variation of genome sizes between different
types of
>>>>>> animal. The distribution is not remotely random.
>>>>> There is much more variation within groups than between them,
except for
>>>>> the lungfishes, and there we're talking about only 3 species; not
much
>>>>> room for variation. Amphibians are the weird ones, but note that
their
>>>>> variation covers the variation of all the other groups except
teleosts.
>>>>> Now phylogeny does make some patterns even if variation is random, as
>>>>> long as it doesn't change too fast. But I don't see anything that
needs
>>>>> a serious causal explanation in that data, nor does it contradict
my claim.
>>>> That "Genome size seems pretty randomly distributed over the tree of
>>>> eukaryotes?" 2.3, 5.7, 90.4, 3.5, 1.2, 16.7, 2.3, 1.5 and 3.5 look
>>>> like a suspiciously non-random bunch of numbers to me.
>>> First, those aren't eukaryotes, but only vertebrates.
>> That was not a complete list of all eukaryotes ;-)
>
> My point is more than that; it's a highly biased list, concentrating on
> one small group, just because you happen to belong to that group.

Actually AFAICR, mainly because it was the first of two sections
on animals in the paper I snipped it from, and I wanted to snip
as much as possible. Perhaps *they* put the vertebrates first for
a reason like the one you suggest, though.

>>> Second, in what way do they look non-random? It would seem that
>>> the distribution is skewed toward the small end; is that what you
meant?
>> No. The outlying samples are too far out.
>
> OK, I'll agree that simple "random walk" makes it unlikely for big
> genomes to be concentrated in a couple of groups. But you also have to
> consider the phylogenetic dependence here. We don't have thousands of
> independent random walks from the starting point. Instead we have a
> branching series of random walks with each new pair of branches
> inheriting its ancestor's genome size. If some frog happens to have an
> unusually large genome, its decendants start with unusually large
> genomes, and some may get even larger, and so on. Anyway, the take-home
> message is that you shouldn't look at these as if they're independent
> samples.

The table looks like reasonable evidence against
a literal interpretation of your "genome size seems
pretty randomly distributed over the tree of eukaryotes".

However, I don't see any conflict between this
data and the idea that genome size is selectively,
neutral - which would be a more sensible claim,
and now looks like what you meant.

No. I meant that there is no obvious directional trend in genome size.
As I get tired of pointing out, this doesn't mean that it has to be
selectively neutral. There may be selection, as long as it fluctuates in
direction.

>> For example if Cavalier-Smith's K-selected organisms are common, there
>> will be a cluster of large genome organisms - and if his r-selected
>> organisms are common, there will be another cluster of small genome
>> ones. Even if the K-selected organisms and r-selected organisms are
>> somehow equal in number, the resulting senome sire distribution from
>> these two types of selection won't look like the results obtained
>> from a random walk.
>
> As I said before, you are manufacturing a dichotomy that does not exist
> in nature; k/r is a continuum.

We are discussing this elsewhere.

>> Genuine neutrality is the best way to produce a random walk.
>>
>> Fluctuating selection can do it in theory, but there had
>> better be a good reason to expect the selective forces to
>> almost exactly cancel each other out, and rarely does this
>> happen.
>
> I'm reminded here of the Central Limit Theorem. Are you acquainted?

No, but:

http://en.wikipedia.org/wiki/Central_limit_theorem

> The combination of many random variables, regardless of their individual
> distributions, tends toward a normal distribution of effect.

Frankly I don't see how you think it applies.

It's a bit of an analogy. A normal distribution is symmetrical about the
mean, even though the contributing distributions may be highly skewed.
Thus many fluctuating selection pressures may produce a symmetrical set
of evolutionary directions, even if there is no reason to believe that
any one cause will balance out.

.