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Biomedical subjects

Y Onishi

Publications and source records attributed to Y Onishi.

At least 163 records · Page 9Linked to original sources
PubMed1974

Genetic analysis of an Escherichia coli mutant with a lesion in stable RNA turnover.

A mutant that rapidly degrades more than 80% of its rRNA and tRNA under defined conditions was genetically analyzed. Two genes, srnA and srnB, are separately located, and the mutated alleles of both are required for degradation of stable RNA in cultures treated with rifampicin at 42 degrees . srnA is closely linked to tsx by matings and transduction tests; by P1 transduction, the gene order is lac (9 min) proC (9.55 min) tsx (9.8 min) srnA (about 10 min) purE (12 min) rnsA (14.4 min). srnB is not yet completely mapped, but is outside the lac-rnsA region, probably in the region between 75 and 90 min.-The product of the rnsA gene, RNase I, is a potent endonuclease of E. coli, and the only one known that can attack ribosomes and tRNA. However, not only are the srn lesions genetically separate from rnsA, but also, derivatives of an srn strain were prepared lacking RNase I, and they retain the Srn(-) phenotype. Thus, no correlation of rapid RNA turnover and RNase I activity has been found.

Alleles↗
PubMed1972

3',5'-cyclic adenosine monophosphate-requiring mutants of Escherichia coli.

Mutants that require exogenous 3',5'-cyclic adenosine monophosphate (cAMP) for exponential growth were isolated from strains deficient in adenyl cyclase. Studies of one strain showed that cAMP is not incorporated into macromolecules; instead, it seems to have a regulatory function, i.e., in media lacking cAMP, cells form ribonucleic acid (RNA) and protein at linear rather than exponential rates. The exact lesion is not known; ribosomes, messenger RNA, and the beta and beta' subunits of RNA polymerase continue to be made in absence of added cAMP.

Adenylyl Cyclases↗
PubMed1971

"Phospholipids of virus-induced membranes in cytoplasm of Escherichia coli.

Infection of Escherichia coli with amber mutants of phage fd, in contrast to infection with wild-type phage, leads to cell death and the proliferation of intracytoplasmic membranes observed in electron micrographs at the poles of the cells. The accumulation of membranes correlates with changes in structural phospholipids, especially a marked increase in the apparent rate of formation and total amount of cardiolipin (from 4 to 20% of total radioactive phospholipids), and a compensating decline in phosphatidylethanolamine.

Autoradiography↗
PubMed1971

Growth inhibition and appearance of the membranous structure in Escherichia coli infected with bacteriophage fd.

Thirty-six mutants of fd, a virus that infects but does not kill Escherichia coli, were isolated; 35 mutants were categorized into six complementation groups. Abortive infection with mutants in genes 1, 3, 4, 5, and 6, but not in gene 2, produced a cessation of host cell growth, generally linked to low burst size and to the formation of aberrant intracytoplasmic membranous structures. The membranous structure was studied during infection with various phage and hosts. Appearance of the membranous structure was linked specifically to incomplete phage maturation at the cell membrane, rather than solely to the inhibition of host cell growth or to infection with mutant phage, since (i) in one host, cell growth was inhibited, but no membranous structure developed; and (ii) when antibody against virus was added to cells infected with wild-type phage, phage extrusion was inhibited, cell growth stopped, and the membranous structure once again developed.

Agar↗