Champe here told further of his efforts to map the rII region of the bacteriophage T2. His goal was to map changes in the
mutant strain rII to changes in the amino acid sequence of the protein for which it coded. (Bacterial viruses are composed
of nucleoprotein, an assembly of nucleic acid and protein, which upon infection enters the bacterial cell, where it induces
the synthesis of more viral nucleoprotein.) Champ was beginning to isolate and purify parts of the polypeptide for which rII
Champ's letter illustrates the degree to which research in molecular genetics depended on collaboration between laboratories
across countries and across continents, on the exchange of researchers, ideas, and experimental strains.
Number of Image Pages:
2 (152,502 Bytes)
1967-03-01 (March 1, 1967)
Original Repository: Wellcome Library for the History and Understanding of Medicine. Francis Harry Compton Crick Papers
Thank you for the UGA manuscript and the mutants you have sent. We can add the following about X655 and UGA barriers: Neither
X655 nor FC (31, 87), which generates b6, produce any detectable component 30 (the peptide of the B cistron we look at).
Incidentally, what happened to the argument of last summer, based on ts and tr revertants of ochre's that suggested UGA
codes for something?
We must take back what we said earlier about the left end of the component 30 region. We had found that (1,38) gave component
30 whereas (1,58) did not, indicating that the left end of the region was between 38 and 58. We then found that other pairs
extending further to the right, e.g. (87,222), gave component 30, but (1,222) did not. This suggested that the lack of component
30 for (1,58) might be due to mb which lies between 38 and 58, and this seems to be the case since (1,58) and (1,222) with
the barrier reverted now give the component. The main moral is that we can't use frame shift pairs to determine the left
end of the region, though they do tell something about where the end is not. Why 1589 doesn't make component 30 I don't
understand except that, of course, in 1589 B cistron translation is controlled by A cistron initiation and there could be
considerably less B made in this case.
The resulting shrinkage of the component 30 region was, in fact, comforting since the behavior of the peptide on Sephadex
and dialysis did not indicate as large a piece as the mapping did.
Purification. By following component 30 we have been able to purify the B protein some 5-10 fold with the result that some
of the clutter of the chromatogram has disappeared, component 30 is more distinct, and other H3-C14 differences appear. When
we are able to at least roughly map one or two of these new peptides I think we will write up what we have. The purification
goes very slowly due to the horrible assay, but we can now do about 10 column runs a week.
Could you send the following mutants
X665 (UAG), I realize this is same as N97 but would like it Kosher.
FC (0, 40, 55, 36, 31, 47);
also I was wondering if you had found any other regions in rII, besides around P83, subject to frame shift suppression.
My student, William McClain, who is the one laboring with rII, says he would like to come to Cambridge on a post-doctoral.
He should get his degree in June or August of this year but I want to keep him the following winter, so he was thinking in
terms of the summer or fall of 1968. If there is a possibility, I will encourage him to start looking into fellowships etc.
I can honestly say that they don't come any better. Not only is he full of ideas but has the experimental ability and
energy to go with it.