From: ian@inf.ethz.ch (Ian)
Newsgroups: sci.nanotech
Subject: Re: Inheritance of acquired characteristics
Date: 28 Sep 92 00:55:44 GMT
Organization: Dept. Informatik, Swiss Federal Institute of Technology (ETH)

In article <Sep.25.17.03.26.1992.22764@planchet.rutgers.edu> efi!chrisp@uunet.uu.net (Chris Phoenix) writes:
>
>I'll go *way* out on a limb and give an example from biology.  I
>assume that protein folding is not a direct function of DNA--a complex
>protein may have two states with enough of a potential barrier between
>them that it will stay in whichever shape it is folded into.  Given
>that assumption, imagine that a ribosome for some reason folds into a
>less compact shape than normal.  This is the "change".  This new shape
>just might prevent proteins from folding like they used to, and the
>effect would be seen more on bigger proteins--like ribosomes.  So it
>seems possible that this change could be inherited in new generations
>of ribosomes manufactured by the original changed ribosome.  But
>certainly cells are not "designed" to inherit such changes.
>

This is not generally observed to happen and, intuitively, I don't expect it
to be very likely (although it has been considered, see (I think) 'The Blind
Watchmaker' by Richerd Dawkins for a non-technical discussion).

I'm not sure why my intuition objects to it but I suspect it's an argument
along the lines of (this is for biology):

i) Can the 'change' be *both* sufficiently energetically stable to pesist
   between generations *and* have a sufficiently high activation barrier
   between it and the 'normal' state that they wouldn't both be expected in
   a typical organism.  (ie can the molecule have two stable states so far
   apart)

ii) If the difference is a property of a single molecule then (a) the first
    'changed' organism will have both forms, and, (b) there's a 
    probabilistic chance that offspring will 'inherit' only one of the forms
    so 'homozygotes' will arize.  Four cases now present themselves:

    -1.  The changed form is at a disadvantage and is eliminated.

    -2.  The normal form is at a disadvantage and is eliminated.

    -3.  The heterozygote is at an advantage or disadvantage, this can
         only be exploited by the organism with additional genetic changes
         which 'intentionally' produce one form or the other.

    -4.  There is not advantage one way or the other, in which case statistical
         drift will eventually eliminate one at random.

iii) (this is the most usefull argument from a nanotech consideration)
     A 'change' occuring just at the point where it can feed-forwards into
     more of itself is actually very unlikely because (a) the presence of the
     specific functions required by 'life' is unlikely and random changes are
     most likely to have no function at all, (b) if a 'changed' object
     does have some effect on other objects then it is most likely to either
     destroy or randomise them and not to specifically reproduce itself, and,
     (c) it's very likely to kill or cripple the system possessing it.

  Having said that, I do know of one possible example of what you suggest
in the world of biology, BSE (Bovine Spongiform Encephalopathy) and the
related diseases (Scrapie (sheep), Kreutsfeld Jacob Syndrome (human, mis-
spelt), Kuru (human, induced by cannibalism):

  In these related conditions, the infective agent is a natural brain protein,
it is not associated with any DNA and no 'chemical' (as opposed to 
conformational) difference can be identified between it and the non-infective
form. (Spooooky :-)  However, the infective agent is an aggregate of large 
numbers of the protein, not found in normal brains.

  (This is something I occaisionally work on, very little is know about any
aspect of it but:)  The most likely (to me) explanation for this condition
(and for various bits of pathology and stuff I havn't mentioned) is that the
protein, in its natural state, is involved in some stage of its own
manufacture. (Not at the ribosome stage, but the protein is post-sythetically
modified and exported from the cell, so there are plenty of places where it
could be involved)  This diseased form can there forew be seen as interfering
with this manufacture and either increasing it or interupting it at a 
'half-finished' stage (victims have huge quantities of the protein in their 
brain-cells). (of course, this theory is exactly equivalent to the protein 
interupting its own degredation as well).

  **BUT**, the important point about BSE is that it (because it arises in
several species (man, sheep, cow, mouse, mink)) must be seen as probably
something that irises as an unfortunate side effect of some essential
aspect of normal life (ie the disease function is only a very slight
corruption of normal function).  If this weren't the case we would have
expected some of the organisms to have drifted sufficiently far apart that
inter-species transmition could not occur (this argument will be stronger
when we know more about which species cannot get it); the implication of
inter-species infectivity (remembering that this isn't an organism in its own
right and so cannot have been selected for crossing species boundaries) is
that the individual species were all 'constrained' to retain the dangerous
system.

  This is obviously a very special case, I woundn't worry about it happening
to nano-systems until it does :-).

p.s Don't eat cows ;->