Spetnerian "information" & its biological application

Tim Ikeda (tikeda@sprintmail.com)
Sun, 27 Sep 1998 13:03:17 -0400

Brian writes:
[...]
>Here I'll try to summarize the argument trying to avoid
>too many details. The reason the information decreases
>is that the immunity is attained due to a decrease in
>specificity. How so? Well, the drug works because the
>mycin molecule is able to fit snugly into a matching site
>on the bacterial ribosome, "like a key fitting into a lock".
>The mutation causes a sufficient change in "shape" of the
>matching site so that the key no longer fits. This is what
>is meant then by the loss of specificity which is presumably
>then a loss in information. Spetner emphasizes that there
>are many mutations which result in this loss of specificity.
[...]

If that's the case then Spetner is having it both ways. In previous
examples given, where an mutated enzyme becomes able to catalyze a
reaction with a new (different) substrate, it was claimed that this
was a decrease in information because the specificity of the enzyme's
active site was reduced (of, this is only with respect to the enzyme's
original substrate). However, in the case of a target enzyme where
a new mutation reduced the binding of an antibiotic, it is again
claimed that this is a reduction in information/specificity. How can
both examples be correct? They can't be unless one is switching the
metrics.

I suggested this in an earlier letter to the group, now archived as:
http://www.calvin.edu/archive/evolution/199809/0063.html

If an antibiotic that normally binds to a site on a target enzyme
can no longer bind to a mutant version of the target, we could
score this as either an increase or decrease of information, depending
on which Spetnerian metric or context we apply. In physical terms,
changes in binding affinities generally means that some of the normal
contact sites between the enzyme and the antibiotic (or some other
molecule) have changed. Changes in the contact sites can affect binding
and catalysis.

On one hand, one could say that some of the binding sites for the anti-
biotic have been lost. If Brian's characterization of Spetner's
argument is correct, then Spetner is claiming that a loss of
binding = loss of information.

On the other hand, one could claim that the target enzyme has acquired
an increase in specificity in that it has acquired a modified binding
site that can now discriminate _against_ the antibiotic molecule. Thus
we could say that the enzyme experienced an increase in specificity
against certain antibiotics.

This becomes more obvious if we take the case of competitive enzyme
inhibitors which bind to the active site of enzymes and thus block the
binding of the enzyme's normal substrate. In these cases the enzyme
lacks the specificity to distinguish between inhibitor and substrate.
There are many cases where mutations have altered the binding contacts
around the active sites of enzymes which prevent the binding of the
inhibitors and thus _increase_ the specificity of the enzyme for its
normal substrates.

The important message from Spetner's examples is that a gain or loss
of Spetnerian "information" seems largely dependent on the _context_
in which the cases are examined. Brian's comment at the end of his
latest post reflects a concern I've had too.

Brian writes:[...]
>OK, let's leave this aside for the moment and address the main
>point I had in mind when bringing up Yockey. When Yockey is
>discussing information content of cytochrome c the information
>content is wrt the normal biological function of the molecule.
>Is this what Spetner is talking about when he says a point
>mutation results in a loss in information? Not unless one
>considers dying when exposed to streptomycin a biological
>function of the bacterial ribosome.
>
>So, if someone wants to insist that the mutation results in a
>loss in information then let them at least be specific about
>what information is being lost. Let them say "the mutation
>resulted in the loss of the information required to die when
>exposed to streptomycin." Stated this way, the observation
>can hardly be considered an objection to evolution ;-).

Regards,
Tim Ikeda
tikeda@sprintmail.hormel.com (despam address before use)