Q39 -
LEDERBERG, ESTHER M., University of Wisconsin, Madison, Wis.--Fine

structure of the Gal loci in Escherichia coli Kel2.e<A distinctive recon
(one of a group of closely linked loci separable by recombination) has
been assigned to each of ten independently occurring Gal” (galactose none
fermenting mutants. All the mutants were obtained after UV irradiation
except Gal, which was spontaneous. Allelism was tested by large scale
matings and by transduction analysis.--Prophage-Linked transduction via
HFT A; where practically every phage particle may result in a transduce
tional event, produced heterogenotic clones when donor and recipient bore
distinctive recons. The heterogenotes were unstable, segregating the two
input and two crossover classes (Morse, Lederberg and Lederberg 1956).
Two cistrons (cisetrans position effect groups) had been demonstrated:
trans heterogenotes with members of the same cistron are phenotypically
mutant. Galactokinase was missing in mutants of one cistron (Gal 2,8)
while UDP transferase activity was absent in the other (Gal 1, 4, 6, 7);
a defect corresponding to human congenital galactosemia, (Kalckar,
Kurahashi 1957). Gal and Galo™ are genetically cistronic with both of
the foregoing groups; they have not yet been successfully analysed for
| their enzymatic defect. Among two hundred new mutants, no recons identical
with the first ten have recurred. Most have been assigned to either of the
first two cistronic groups, but a small number which would represent a
fourth genetic group have given only normal galactose-positive heterogenotes

with every standard Gal” tested. A few mutants were not transformable by »
but were found to carry other modifiers including that of hexose metabolisn
which obscure their relationship to the Gal” group.--An attempt was made to ms

the Gal markers in linear sequence by their relationship -
to the Lp locus. Intercrosses of Hfr M Gal, x F Gal, were made on

a medium which selected efficiently for u*Gal,*ca1,* recombinants, and

these were then scored for the segregation of an Lp marker. However, the
linkage of GaleLp proved te be not close enough to compensate for the pere
turbations of segmental loss from the Hfr parent, and the data were indeu

cisive,.

LOth International Congress of Genetics, Montreal, 1958.