Thank you for cultures "40a" (Cushing) of sulfonamide resistant Neurospora. They have just arrived, and in good condition.
Your comment that this strain is probably not an exceptional pab producer makes it unlikely that there is any direct bearing
on my pab-adaptation work. However, I expect to try the following exps. E1633 plus represents adapted 1633; 1633 plus is wild
type; C40a plus your SA-resistant.
1. Compare pab production of E plus, 1633 plus and C40 plus on minimal.
2. Behavior of C40-1633 minus types, obtained by crossing. It will be interesting to determine the response of these double
mutants to pab-SA mixtures.
3. Possibly, effects of C40 plus on sulfanilamide-cultures medium. (growth of 1633 plus, 1633 minus on culture filtrates):
"is sulfa destroyed."
There are several disquieting points in your letter. It would help me greatly if you could clear these up:
1. Inhibition by PAB! Is wild type inhibited by PAB? Is C40? (at what concentrations.
2. Stability of C40 on minimal? What can I keep in on, that will support growth of Wild Type?
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About E1633. There isn't much to say. It seems to mutate rather readily back to the pab-less type in some cross. A linkage
to the 1633 locus is deperately [sic] required; at present, because of this mutability I cannot assure myself that E1633 is
or is not allelic to 1633. It had not occurred to me to compare frequency of 2nd division segregation of E plus/E minus, as
you suggested for your SA-resistance gene.
(These mutability compels me to revise my former conclusion, based on the results of E plus x Wild Type crosses, that E was
not allelic with 1633.)
A number of people are fundamentally interested in sulfonamide-resistance here at the Columbia Medical School. If I can persuade
them to work on Neurospora, something may come out on the mechanism of the resistance. I shall, of course, refer them to Dr.
Cushing and yourself, "prima facie." [mark to note, (N.B. -- no longer A.S. USNR.)