Gene expression and cell cycle regulation.
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Cell Cycle↗
Biomedical subjects
S J Hochhauser
Publications and source records attributed to S J Hochhauser.
Regulation of gene expression in normal and neoplastic cells - a review.
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Animals↗
Escherichia coli mutants deficient in deoxyuridine triphosphatase.
Mutants deficient in deoxyuridine triphosphatase (dUTPase) were identified by enzyme assays of randomly chosen heavily mutagenized clones. Five mutants of independent origin were obtained. One mutant produced a thermolabile enzyme, and it was presumed to have a mutation in the structural gene for dUTPase, designated dut. The most deficient mutant had the following associated phenotypes: less than 1% of parental dUTPase activity, prolonged generation time, increased sensitivity to 5'-fluorodeoxyuridine, increased rate of spontaneous mutation, increased rate of recombination (hyper-Rec), an inhibition of growth in the presence of 2 mM uracil, and a decreased ability to support the growth of phage P1 (but not T4 or lambda). This mutation also appeared to be incompatible with pyrE mutations. A revertant selected by its faster growth had regained dUTPase activity and lost its hyper-Rec phenotype. Many of the properties of the dut mutants are compatible with their presumed increased incorporation of uracil into DNA and the subsequent transient breakage of the DNA by excision repair.
Coliphages↗
Genetic mapping of xthA, the structural gene for exonuclease III in Escherichia coli K-12.
The genes xthA, pncA, and pabB were ordered relative to others by two- and three-factor transductional crosses with bacteriophage P1. The genes studied span 2 min (2%) of the genetic map of Escherichia coli K-12 in the clockwise sequence pheS-pfkB-xthA-pncA-gap-pabB-fadD. Eleven independently derived xth mutations were examined; all were known to affect exonuclease III and its associated endonuclease II activity, and all were mapped in the xthA region. pncA mutations were found to confer resistance to 6-aminonicotinamide, whereas some pheS mutations are known to specify resistance to p-fluorphenylalanine. xth mutations were readily transferred into other strains by selecting for these co-transducible drug resistance markers.
6-Aminonicotinamide↗