Darwin and Hiroshima

mcdonald at wsuhub.uc.twsu.edu mcdonald at wsuhub.uc.twsu.edu
Tue Dec 27 10:21:32 EST 1994


>When I read about the process of evolution (years ago), I was lead to
>believe that random mutations in genes were part of the engine of
>evolution. I thought I read that nonionizing radiation was the cause of
>these mutations.                 ^^^^^^^^^^^

>But I'm confused now because it is reputed that the children of the
>victims of Hiroshima show no higher level of birth defects normal.

>What am I missing?

Here are my thoughts on several things you are missing...

1) Radiation has been a source of mutations throughout the
evolution of life on Earth.  However, this radiation comes in
numerous forms and many of them are ionizing (e.g., cosmic rays
from outer space, natural radiation sources in our environment).
It is not, however, the only source.  The enzymatic machinary
that copies and repairs our genome sometimes makes errors.
Further, there are a number of nonradioactive agents in our
environment that can increase the error rate.  Radiation is only
one slice of the mutation pie.

2) Another thing that you are missing is time, time, and plenty
of time.  The remarkable changes that we see in the history of
life on this planet area product of the acquisition
of mutations over mind-bogglingly large expanses of time.
Speaking evolutionarily, the time that has elapsed since
Hiroshima is inconsequential for the purposes of evolution.

3) One other important difference that needs to be taken into
account when you are thinking about Hiroshima as a microcosm
of evolution are what "mutagenologists" call endpoints.  In
evolution the endpoint is usually survival in a changing
environment.  Here, a random mutation may have no readily
observable effect on the offspring but can confer a selective
advantage should environmental conditions take a certain turn.
In the Hiroshima study by comparison, the endpoints examined
were much less subtle.  Looking for readily observable birth defects
in the several generations of offspring deriving from exposed
persons examines only for a small subset of possible mutations
(i.e., probably dominant and having an easily detectable
phenotypic effect).

Dave McDonald
Assistant Professor of Biology
Wichita State University




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