Complexity

Chris Cogan (ccogan@sfo.com)
Mon, 29 Nov 1999 14:12:28 -0800

> Chris:
>
> >>How does complexity come about?
> > >>Complexity increases by variations, some of which themselves
> > >produce even more-complex variations.
>
> Susan:
>
> >> what Chris talks about above has been observed to occur and isn't
> >>controversial.
>
> Me:
>
> >What observations do you have in mind? (I hope you are not confusing
> >observation with inference).
>
> Susan replies:
>
> >this is from the much-maligned talk.origins website:
>
> >"[An] obvious increase in information can occur when a gene duplicates
> >and the two copies undergo independent mutations leading to two genes
with
> >somewhat different functions.
>
> I agree that this can happen and probably has happened. But is this
> really the mechanism behind the origin of so many new genes?

Chris
It's *one* mechanism. Genes can also recombine in ways to form new genes.
The copying mechanism is, at best, sloppy. In sexual reproduction, it's
almost guaranteed to produce novelties fairly quickly and often, to
introduce *new* genes until the gene pool is *so* large that nearly single
all new genes possible and viable have been created (but increasing the
population *also* increases the chances of *new* new genes being created out
of "old" new genes). If an Okapi with a longer neck breeds with an Okapi
with a stronger heart, you'll probably get some Okapi's with *both* a longer
neck *and* a stronger heart.

Mike
> I
> am quite familiar with this textbook model, enough so to realize
> that it is not very robust in that it simply ignores the obstacles
> to the duplication-functional divergence proposals and merely assumes
> they were overcome. Thus, it's not a question of whether this
> can occur. It's a question of whether this was really the driving
> mechanism.

Chris
Why assume that there is such a thing as *the* driving mechanism, except at
a very high level of abstraction? We know as an observational fact that
genes can change and come into being in a number of different ways
(duplication is one). Why assume that such a specific process must be *the*
driving mechanism? Why can't there be any number of different mechanisms up
to whatever limit is set by genetic chemistry? Duplication, duplication with
modification, deletions, transpositions, replacements, should all be
possible, along with variations in levels of redundancy,
conditionally-active genes, genes that allow a codon or two to switch
*other* genes on or off, genes that "select" one gene to make active from a
"list" of genes, genes that cause other genes to be skipped, genes that
cause other genes to be interpreted differently, and so on, all seem to be
possible (and some are known to occur).

Note that, as the genomes come to have more of such "gene control"
mechanisms, the degree of change between generations can increase. In
principle, it might even be *possible* (though not likely) for one gene to
switch what amount to whole genomes on or off, so that the offspring of an
organism *could* be radically different from the parent organism (at least
relative to what we do in fact see). Thus, the offspring could be different
in *major* morphological ways, but differ *genetically* in as few as *one*
control gene. This is also why Gould's view that major evolutionary changes
can occur in a (*relatively*) short period of time is very plausible to me.
Organisms with a significant gene "library" can make major morphological
changes by making very small *genetic* changes.

Why is this possible? It's possible because there is no simple one-to-one
mapping between genetic material and the organism's morphological features.
Genes store information in what amounts to a kind of computer program that
begins execution at replication time and continues throughout the life of
the organism. As the Mandelbrot set and any number of *genetic* examples
show, such programs, whether in real computers or in organisms, can often
generate large and complex results from a *small* initial "program."

And, of course, that small program may be derived from one that did *not*
produce such a result, and it can be derived by a very small additional bit
of "programming." Consider the following:

1. Let A = 1
2. Let A = A + A

Simple, isn't it? Also, it doesn't do much. But, consider the following:

1. Let A = 1
2. For B=1 to 1000000
3. Let A = A + A
4. End

Now, the result is large, but the program is still quite small. Such
repetitive processes could cause a nerve ganglion to become a brain (though
probably not a fully functional brain). Subsequent generations could "clean"
up the result and make it work better than it did initially. I chose the
brain example because it's an example of a fairly complex structure built on
a fairly simple "template," apparently by a repetitive process.

> >Gene duplication, mutation and selection are all known to occur
> >due to natural biochemical processes in a variety of organisms studied
> >in the laboratory.
>
Mike
> What variety of organisms has this been observed in? What genes
> and what functions is this author talking about?

Chris
Yeast, bacteria, and probably many others. Yeast genes duplicated so as to
produce better sugar-scavenging. New genes were produced to help bacteria
deal with a too-warm environment.

>
> >Many gene families are known with members that encode proteins
> >having related structure and related but distinct function. Each family
can
> >be explained by multiple gene duplications followed by random
> >mutation and differentiation of the functions of the individual gene
> >copies.
>
> This is an inference, not an observation. That something can be
> explained in light of this model is hardly surprising given that
> the model is so vague.

No, I don't think it's an inference, unless you mean that scientists did not
actually *see* each individual codon being laid down. It's not particularly
vague, either. A duplicate gene or cluster of genes is observationally
*specific*, as is their variation over subsequent generations, etc. That it
is "random" is not really an inference either; it's a statistical
generalization of observations. If it is *not* random (within the limits set
by physics and chemistry), we have no *evidence* that it is not.

> What is almost always missing from
> these explanations is independent evidence that the model
> correctly interprets the data. Typically what you have is this:
>
> Two genes are found that are similar. Similarity is interpreted
> to mean genetic relatedness. The differences are interpreted
> to arise from divergence after duplication. The mutations
> and differentiation of functions, along with the selective
> advantages associated with them, are unknown and simply
> exist in the realm of vague imagination. None of this means
> the model-explanations are incorrect, but I think it important
> to realize we are dealing with explanation that may sound
> more rigorous than they really are.

That sounds *fairly* rigorous to me. But I'm not talking about that when I'm
referring to laboratory observations. If one organism is found to have a
gene, and it divides into an two organisms, one of which has that exact same
gene *except* for a small modification, I'd say that it was pretty well
shown that that new gene was a variation on the old one. The alternative is
that some mysterious force reached in and made a new gene that just
*happened* to be a near-perfect duplicate of the gene in that location in
the parent genome. Perhaps you are forgetting that the *function* of genes
during reproduction is: *to be duplicated*.

Besides, we already know that genes *are* modified during replication. Do
you think that a *new* gene created by accident by an extra duplication of
an existing gene *won't* be subject to the same modification processes as
existing genes? If this is what you think, then I must ask: Why? Is there
some mysterious force-field around new genes that prevents them from being
modified like any *other* genes might be? Is there something to keep them
from getting recombined with other genes during sexual reproduction? Is
there any reason even to *suspect* that such a fact is the case? What
observational facts would require such a bizarre hypothesis? Are there
*known* instances in which such new genes were replicated many zillions of
times *without* modification?
>
> >Clearly the expansion from a single primordial gene to a large
> >family of genes with distinct functions represents an increase
> >in genetic information."
>
> I would tend to agree, however, with two caveats. First,
> increasing the amount of genetic information does not
> necessarily correlate with an increase in organismal complexity.
> Secondly, as far as I know, such expansions are all
> inferences and not observations.
>
> Chris also replied to my request with the following:
>
> >For just two examples: the increase in genes of yeast forced to live for
> >many generations in a low-sugar environment, the increase in genes in
> >bacteria forced to live in an environment that's too warm for them, etc.
>
> Without references for these claims, I can not reasonably discuss
> them or their significance. Perhaps Chris can supply those
> references. Furthermore, while he is at it, I note that he gives
> the impression there are many such examples (since these are
> just two and the list is followed with "etc."). Given that
> Chris seems knowledgeable about this area and probably has
> a longer list of obervations in mind, perhaps he can also pick
> the five most impressive examples of these observed examples
> of increasing complexity.

I'm not especially knowledgeable, but I have heard of other instances over
the years. Susan posted a paper on the information increase some time ago.
I'll repost it in my next post (to keep the size of this one reasonable).