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Biomedical subjects

Y Hirota

Publications and source records attributed to Y Hirota.

At least 631 records · Page 35Linked to original sources
PubMed1970

On the process of cellular division in Escherichia coli. V. Incorporation of deoxynucleoside triphosphates by DNA thermosensitive mutants of Escherichia coli also lacking DNA polymerase activity.

Double mutants of Escherichia coli were constructed by combining DNA thermosensitive mutations affecting either DNA initiation (DnaA) or elongation (DnaB) with the Pol A1 mutation, which abolishes DNA polymerase activity. Incorporation of labeled deoxynucleoside triphosphates was studied in these mutants using toluene-treated cells. This incorporation was found to be exactly correlated with the capacity of the mutants to synthesize DNA in vivo.

DNA Nucleotidyltransferases↗
PubMed1966

Gene recombination and segregation of resistance factor R in Escherichia coli.

Hashimoto, Hajime (Osaka University, Osaka, Japan), and Yukinori Hirota. Gene recombination and segregation of resistance factor R in Escherichia coli. J. Bacteriol. 91:51-62. 1966.-Independent chloramphenicol-sensitive (CM(s)) mutants of the drug-resistance factor R were isolated. Introduction of two different R factor CM(s) mutants into a single bacterium, by conjugation or transduction, gave chloramphenicol-resistant (CM(r)) colonies when such strains were plated on a medium containing chloramphenicol (Cm). These CM(r) colonies resulted from recombination between two R factors contained within the same cell. Most of the CM(r) colonies were heterogeneous, and segregation of drug-resistance markers was observed among the progeny. Segregated bacteria which still carried the recombinant R factor were stable for resistance to Cm as well as for other markers of R. All the markers of recombinant R factors were cotransducible with high coincidence and at the same frequency as wild-type R. Sensitive mutants of R which had lost all the resistance markers of the R factor were found also. A mutation of R, referred to as SMA, which was sensitive to streptomycin and sulfanilamide, was capable of reverting to resistance to both of these drugs simultaneously. The sensitive alleles for SMA, CM, and TC were shown to be recessive to the resistance alleles. Mutants of R having multisite mutations or deletions in the CM gene were isolated and used to analyze the pattern of linked segregation of unselected markers of the recombinant R factor. The drug resistance factor R was shown to have two linkage groups, CM-SMA and TC-m.

Chloramphenicol↗
PubMed1966

Loss and repair of conjugal fertility and infectivity of the resistance factor and sex factor in Escherichia coli.

Hirota, Yukinori (University of Osaka, Osaka, Japan), Toshio Fujii, and Yukinobu Nishimura. Loss and repair of conjugal fertility and infectivity of the resistance factor and sex factor in Escherichia coli. J. Bacteriol. 91:1298-1304. 1966.-The drug-resistance factor, R, and the sex factor, F, have homologous traits, including contagious transmission, mediation of sexuality of the host cell, and autonomous replication in their host bacteria. Cooperation between F and R factors was found with a mutant R factor, which is nontransmissible in F(-) bacteria, becoming transmissible when introduced into bacteria carrying F. Conversely, the chromosome of a sterile male strain carrying the mutant sex factor, F(r), becomes transmissible when an R factor is introduced into the cell. The genetic determinants of R factors have been analyzed by isolation of mutant R factors, by sexual conjugation of the host bacteria, and by transduction of R factors with phage P1kc. The fertility determinant of the R factor, m, is inseparable from the determinant for its infectivity, but can be separated from the loci for autonomous replication of the R factor. R and F thus carry genetic determinants governing the same functions.

Acridines↗