June 13, 1958

Dr, Jack L, Strominger

The Edward Mallinckrodt
Department of Pharmacology
Washington University

Euclid Avermme and Kingshighway
Saint Louis, Missouri

Dear Jacks
Forgive me for having delayed so long in answering

your letter of March 15 ~ there are the usual excuses ari not
much to say. Also, perhaps unfortunately, between the time I

last saw you ami your letter we got onto some different taske, (y
but have not altogether abandoned the wall mutant problem, ~\
We have not had much luck still in finding »utants =
for other metabolites besides DAP, If anything turns up, we'll ~>
let you know pdq. We have some new methodological angles to try Ss
out. x
You have the principal DAP mutants already, W3231 is ‘
Davis! 173-25, and essentially equivalent’ to Work's strain too, Q
W3652 is representative of om of our new mutantas I will dig ~

out some more of the rest. I never have gotten McCilvery's
second mutant, have you?

Davis has mentioned that DAP protoplasts became more
resistant to lysis with time, xt if you prepare them quickly
in broth, they are mch more fragile, I argue with you of
coum#éEbout Pardee and Trucco,

I hope you will have forgiven my neglect and keep me
in touch,

By the way, we have a mutant now (Galg) which Kalckar
says is deficient in the epimerase ag well as the first two
enzymes, Ye means to make the obvious inquiry whether galactose
4s still present in the cell walle, (The mutant does not re-
quire galactose for growth after all, Heyond this can you see
any application to the wall problem?)
Dr, Jack L, Strominger
Page 2 = June 13, 1958

Do you know how glucosamine is metabolized by E.
coli? If it goes through UDPGa -» UDPG would it be profit-
able to look for a glucosamine-negative mutant? Or would we
have to feed it UDPGa rather than Ga? Any information on
the utilisation of UDP conjugates by intact cells?

Yours,

Josham Lederberg
Professor of Medical Genetics

JL/ew