Anyway, here is the reply I recieved this morning from Joseph. Art, I did not tell him what your background was, so that explains his explanation of the culture techniques of which you, ( but not me) were already perfectly aware.
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"I would like to preface my remarks on your friend's comments by
noting that I had identified this (and the bacterial cases that
followed) as being ambiguous cases due to the lack of sexuality
in these critters. In the Chlorococcales species (and higher taxa)
have generally been delimited by morphology. The multicellular-
unicellular distinction is generally a genus to family level trait.
Now if by comparing this to the peppered moth, your friend contends
that this phenomenon represents a case of natural selection, he is
certainly correct. IMHO, this is alone doesn't really affect the
question of whether this represents a speciation.
I suspect that your friend is probably arguing that this resulted
from selection acting to increase the frequency of a rare, but
pre-existing, genotype in the population rather than resulting from
selection for a mutant that occurred in the chemostat after the
predator had been introduced. This is a very difficult question
to examine.
I am a student of M. E. Boraas, so I'm familiar with the techniques
used in this work. This particular alga is about 2 - 4 um in diameter.
When we grow them in a chemostat (without the predator) we get a density
on the order of 3 X 10 ^ 7 cells per ml! If a pre-existing variant is
present at a frequency of 0.0001 we would, on average, see it only
once in 10,000 counted. To be sure of catching it at this frequency,
we would have to count an incedible amount of cells! (Just as a point
of information, when we do direct counts, we usually count 300-500 cells
in a sample. This is in accord with phycological and bacteriolgical
practice).
I will also make the argument that quite a bit of mutation does go
on in a chemostat setting. In the early 1970's Kubitchek (sp?)
reinterpreted some of Novick and Szilard's E. coli chemostat data.
What N & V had done, was to grow E. coli continuously in the absence
of any bacteriophage. Periodically they did plate counts for resistance
of the bacteria to phage T5. In a bacterial population of about
3 X 10 ^ 8 cells per ml, they found there was a fluctuating level of
T5 resistant cells. This level fluctuated between 10 ^ 2 and 10 ^ 3
cells per ml. A graph of this over time would look like:
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with time as the x-axis and T5 resistant cells as the y-axis. (Note:
the above graph is diagrammatic. I will send you the citings for
Kubitchek's stuff. I don't have it handy right now.)
Kubitchek interpreted this as the result of a series of mutations in
the chemostat. The increase of T5 resistant cells results from a
mutation that makes a T5 resistant genotype the fastest growing
genotype in the vessel. The decrease results from a mutation making
a nonresistant genotype the fastest growing strain. Now, I don't
know whether you or your friend are familiar with chemostats, so keep
two things in mind:
1) After an initial transient phase, a single population
in a chemostat is in steady state. Growth (in terms of
number of cells) is balance by cells washing out of the
vessel.
2) The population in the above work originated as a single
cell grown up to fill the vessel. All strain differences
result from mutations occurring in the vessel or during
the growth to produce the cells to innoculate the vessel.
I don't know if this addresses your questions. The address above
should work for e-mail. I'm around and will try to respond promptly.
I'll get you citing in the next letter.
Joe
Joseph Boxhorn ()
Department of Biological Sciences University of Wisconsin--Milwaukee
"Coffee does not make you nervous - your own inadequacies do this.