>Other examples would include intragenic and intergenic supressors,
>which are far more common than reverse mutations. Of course,
>one could argue that these types of mutations restore the level
>of information to its initial state, that is, it's an increase relative
>to an earlier loss (thus it may not be a net increase).
Tim replied:
>On occassion, Spetner sweeps this under the rug by using that
>argument. Other times, he invokes "directed mutations" as the
>explanation -- That the genome is programmed to respond in
>that way.
I can't really comment as I have not read Spetner's book. But
if he claims that no mutation can increase genomic information,
I don't agree. But I'm not sure this is the important point.
If Spetner wants to paint himself in a box where "no mutations
increase genomic information," the dispute boils down to
finding a single example as you have provided. Yet the history
of life, full of contingency, cannot be boiled down to any single
example.
Here's how I see it. At some point, life emerges. Yet life is information
and where did this information come from? The information-generating
examples I have seen invoke genetic variation coupled to selection
(back to Darwin). But all of this presupposes life which itself
presupposes information. Paul Davies nicely outlines this problem
and finds that, as a physicist, when he enters the world of molecular
biology, he finds himself in unfamiliar territory. How did a dumb
planet make a cell? Planets make mountains, clouds, oceans,
atmospheres, but a cell?
After this, a second problem arises. After life emerges, the information
necessary for all life is found in this initial genome. Since then, the
the information necessary for all life is found in millions of different
genomes which, together, represent a HUGE increase since this initial
state. Are the processes of mutation and recombination sufficient for
this immense increase? I don't know. I certainly will not, like Spetner,
assert the answer is no. But neither can I assert the answer is yes.
>Another example of possible information increase:
>There is the case where bacterial strains acquired antibiotic
>resistance and later acquire secondary suppresoor mutations which
>allowed the resistant strains to compete effectively with the
>orginal, non-resistant strain in the absence of the antibiotic.
Sounds good to me.
>What I have seen among those who deny the examples we've given
>is the claim that these mutations result in non-normal proteins,
>abnormal responses or etc. The implication somehow being that divergence
>from "normality" constitutes a loss of information. But that's only
>if we define a particular state (the normal one) as having the
>most "information".
I agree. If one is going to make a strong claim about the ability or
inability to increase information, you need some well-defined parameters
and consensus about specifics. And until we get more genomic data,
I suspect a truly robust analysis is out of reach. Nevertheless, I
do think enough data exist to comment on general trends.
I wrote:
>I personally think mutations that are selected can indeed increase
>information (especially when coupled to gene duplication), but I
>wonder if it's really a piss poor mechanism. If it is, and given that
>life is loaded with tons of information, there may be something solid
>behind all this informational chest-thumping.
Tim replied:
>Hard to say. It's not currently possible to track what happened
>before the rise of the last common ancestor of all life. However,
>given that we can often see relationships between extant sequences,
>I don't think it's too far of a stretch to suppose that many of
>the mutational & recombinational mechanisms we've observed could
>contribute to much of the subsequent evolution.
I understand, but this is all back to subjective impressions. For
example, is a eucaryotic cell truly the result of applying mutational
and recombinational mechanisms to a procaryote? For example,
a recent review from _Cell_ outlines the manner in which the very
logic of gene expression is opposite in the two cell types.
Or consider that procaryotes have been mutating and recombining
for billions of years yet the amount of information increase since
their LCA appears insignificant compared to the lineage leading
to mammals (for example). It amazes me how eucaryotes
ever emerged from a set of genetic and environment dynamics that
have entrapped billions of procaryotes for billions of years.
>For abiogenesis, I think there's a good reason for "informational
>chest thumping". For subsequent evolution, that case is much weaker.
I agree with you here. For abiogenesis, the information-generating
processes used by evolution don't really exist.
>However, most creationists such as Spetner and our friends at the
>Discovery Institute maintain that the bridge from apes to humans is
>too great to be spanned by natural mechanisms; that the information
>necessary to add the an ape's genome is too great. I would like to ask
>them to point out the specific "information increases" needed for
>ape -> human evolution, as reflected in specific protein and DNA
>sequences. Once done, then we can debate.
Yes, this is a good question and hopefully I'll to see the day when
we have genomes from both humans and apes. But I'm afraid even
then it won't be so simple. Information digitally encoded in DNA is
easy to handle and process. But I think biotic information exists
that is not obviously encoded in this manner. The eucaryotic
cytoskeleton clearly plays a specifying role in determining intracellular
location and organization, yet it's hard to see how this stems from the
amino acid sequences of tubulin and actin (I suspect that some
day, the MTOC might be recognized to be far more important than
we think). And then there is the issue of the timing of expression.
When cells divide, daughter cells not only inherit DNA, but also the
cytoplasmic components of the mother cell, including a set of previously
expressed genes (which probably sets the timing). The complexity
of life can truly make one dizzy and should never be underestimated.
For example, I remember learning all about glycolysis in biochemisty
and muscle contraction in physiology; no one had a clue or suspicion
that glycolytic enzymes are mounted on the fibers of the sarcomere!
As with humans and apes, what determines the trillions of neuronal
connections that define the human brain and in what way is this wiring
different from the apes (it must be significantly different in light of the
impressive cognitive differences)? Will genomic and proteome data
answer these questions? Again, I have no idea.
Mike