An azaserine-resistant derivative of Escherichia coli B/UV, AZA/Rl, was found to carry a mutator gene. This gene, designated mutSI, was mapped by means of conjugation and Plkc-mediated transduction. The mutSI gene was cotransduced with argB at a frequency of 2.4%; the gene order in this region of the chromosome is thy argB mutSl. To determine whether a relationship commonly exists between azaserine resistance and the mutator property, 12 additional azaserine-resistant derivatives of B/UV were developed and tested for the mutator phenotype. None of the twelve was a mutator strain. The level of azaserine resistance was not increased over that of the recipient parent when mutSl was transduced to an azaserine-susceptible strain. Reversion studies indicated that mutSl induced adenosine-ribo
Twenty-one Mut mutants were obtained from
Escherichia coli
B (B/UV) and K-12 (JC355) after treatment with mutagens. These Mut strains are characterized by rates of mutation to streptomycin resistance and T-phase resistance which are significantly higher than the parental (Mut
+
) rates. Mutator genes in 12 strains have been mapped at three locations on the
E. coli
chromosome: one close to the
leu
locus; five close to the
purA
locus; and six close to
cysC
. In addition, eight mutator strains derived from
E. coli
B/UV are still unmapped. Some effort was made to deduce the mode of action of the mutator genes. These isolates have been examined for possible defects in deoxyribonucleic acid repair mechanisms (dark repair of ultraviolet damage, host-cell reactivation, recombination ability, repair of mitomycin C damage). By using transductional analysis, it was found that the ultraviolet sensitivity of NTG119 and its mutator property results from two separate but closely linked mutations. PurA
+
transductants that receive
mut
from NTG119 or NTG35 are all more sensitive to mitomycin C than is the PurA recipient. Unless transduction selects for sensitivity, a probable interpretation is that defective repair of mitomycin C-induced damage is related to the mode of action of
mut
in these transductants and the donor. Abnormal purine synthesis may be involved in the mutability of some strains with cotransduction of the mutator properly and
purA
(100% cotransduction for NTG119). Three mutators are recombination-deficient and may have a defective step in recombination repair. One maps near three
rec
genes close to
cysC
.
When animals of the same species are mated inter se it may usually be assumed that they will be fertile and that their progeny will be indicative of a random union of gametes. Dobrovolskaia-%am-adskaia and KoboxoefT ( '32) and later Koboziefl ( '35) have described t~7 0 mutations, t" and t', having ti11 apparent effect 011 segregation in the male mouse (Chcsley and Duiin, '36 ; Dunn and Gluecksohn-Schoenheimer, '39).Males heterozygous f o r either t" or tl transmit the mutation to their of'fspring with a frequency significantly greater than may be expected on an orthodox Mendelian basis.Both to and t' are at the locus of Brachy ( T ) , the factor for dominant short tail discovered by nobrovolskaia-Za~~~a~slrRia ( '27) and studied embryologically in the hcterozygous and lethal homozygous condition by Chesley ( '35). If t' is combined with T the resulting mice are tailless. When mated together T/tl animals (line 29) produce only tailless progeny through the operation of a system of balanced lethals as first described by Muller ( '18) in Drosophila. T/to (line A) mice are also tailless and true breeding. Males with normal tails (to/tl) may be obtained by crossing line A by line 29 and are com-'Submitted in partial fulfillment of the requirements for the degree of Doctor
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