A. D. Hershey, M. Delbruck, A. H. Doermann, and S. E. Luria
March 14, 1946
A. Virus Strains
From the original PC stock of Bronfenbrenner, Kalmanson isolated from a single plaque his PC: This will be called T2K. From
this Luria and Delbruck isolated in 1942 from a single plaque their gamma. This will be called T2L. T2 without qualification
shall mean T2L.
From the original Bronfenbrenner PC Hershey isolated by picking a single plaque his "P9H", characterized by the fact
that it is less well absorbed. This will be called T2M.
These three strains are presumably mutants of one stock. They are differentiated by host range.
Hershey has one other stock, serologically related but of independent origin. This will be called T 16.
These four strains are differentiated by host range. Hershey has isolated the following indicator strains:
B/2L, 2K, 2H
The last mutant of B is the one most commonly found.
B. "r" Mutants
All these "wild-type" strains show lysis inhibition in the adsorption tube. From all of them can be isolated a mutant
without lysis inhibition (or with much less lysis inhibition). These mutants without lysis inhibition also give bigger plaques,
or at least plaques with a clearer halo. These mutants will be designated as "r" (for "rapid lysis in the adsorption
tube"). Thus T2Kr, T2Lr, etc. If it is desired to indicate specifically that one is referring to a wild type stock reasonably
free of the "r" mutant, one should write T2K+r, T2L+r, etc.
No appreciable difference has been found in one-step growth experiments between "+r" and "r" strains.
No serological difference between 2 L, 2K, 2H has been found.
T4, T6, T 16 are different from the above (Hershey).
T4 differs from T6 (Delbruck).
There has never been found a host range difference on mutants of B between any +r and its corresponding "r". However,
the efficiency of plating (e.o.p.) may differ for a "+r" strain and its corresponding "r" mutant. Luria has
found a host range difference between T2+r and T2r, on two strains of dysentery, V 75 and V Weil.
Spontaneously only the mutation from "+r" to "r" seems to occur, i.e., one can pick the "r" mutant
from almost all seemingly pure wild-type stocks, while the "r" stocks seem to stay pure. (Induced mutations occur
in both directions).
C. Host Range Mutants
By plating a virus strain on a bacterial strain resistant to it an "h" mutant is picked up. This resistant strain
may be either a mutant of the original host, or an independent bacterial strain. Both T1 and the even viruses give two types
of "h" mutants, namely,
ht (t for turbid), forming turbid plaques on the new host, and also having an e.o.p. on the new host only about 20% of the
e.o.p. on B.
hc (c for clear), forming clear plaques on the new host, and having an e.o.p. on the new host close to their e.o.p. on B.
(The distinction between plaques of hc and ht can only be made on layer plates, not on spread plates).
The hc and ht mutants are fairly stable. T2H on B/2H throws the two types with about equal frequency. T2K and T1 throw ht
much more frequently that hc.
(Luria feels doubtful, from his results, as to the validity of the distinction between hc and ht mutants).
In some cases it may be necessary to indicate on which host the h mutant was isolated. This should be done by adding the name
of the host in brackets, thus, for instance:
T2Hht (B/2, 2H)
The wild type should again be designated, if necessary, by "+h".
The "r" locus and "h" locus mutate independently.
Whether hc and ht represent independent mutations has not yet been decided.