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Biomedical subjects

M Levine

Publications and source records attributed to M Levine.

At least 595 records · Page 33Linked to original sources
PubMed1971

A portal blood factor as the humoral agent in liver regeneration.

It was demonstrated, by use of extracorporeal cross-circulation, that a humoral factor responsible for liver regeneration does not arise from the liver remnant. While intact livers of normal rats incorporated [methyl-(3)H]- thymidine in proportion to the amount of liver removed in the partner, the greatest response occurred after a total hepatectomy. Evidence from portacaval-shunted,partially hepatectomized animals connected to normal members indicates that the factor is in portal blood and that the onset of regeneration is the result of a quantitative imbalance between the available portal blood factor and the number of liver cells present.

Animals↗
PubMed1971

Virulent mutants of bacteriophage p22.I. Isolation and genetic analysis.

Mutants of phage P22 which form plaques on a P22 lysogen have been isolated. These virulent mutants have been classified into three groups. (i) VirA mutants arise spontaneously in wild-type stocks and form very small turbid plaques on a P22 lysogen. The single mutation responsible for VirA virulence maps near the mnt locus, one of the immunity regions of phage P22. (ii) VirB mutants do not arise spontaneously and have been isolated only from mutagenized P22 stocks. VirB mutants form small, clear plaques on a P22 lysogen. One of the VirB mutants, virB-3, was analyzed in detail. The virB-3 mutant is comprised of two mutations: K5, which maps within the c(2) gene, and Vx, which maps in the region between the c(2) and c(3) genes. Phages carrying either the K5 or Vx mutation are not virulent in themselves but mutate to VirB virulence at a frequency of 10(-5) to 10(-6). It is concluded that K5 and Vx are mutations at specific sites which together confer the ability to undergo phage development in the presence of repressor. (iii) VirC mutants are defined by a large clear plaque morphology when plated on a P22 lysogen. VirC mutants are comprised of the determinants of both VirA and VirB virulence.

Adenine↗
PubMed1971

Superinfection exclusion by P22 prophage and the replication complex.

Wild-type sie(+) P22 prophage converted Salmonella typhimurium lysogens to exclude deoxyribonucleic acid (DNA) injected by superinfecting phage. DNA from a P22 superinfecting virulent phage associated with the replication complex in a sie(-) lysogen but not in a sie(+) lysogen.

Centrifugation, Density Gradient↗
PubMed1970

Control of the replication complex of bacteriophage P22.

A replication complex for the vegetative synthesis of the deoxyribonucleic acid (DNA) of the temperate phage P22 previously has been described. This complex is an association of parental phage DNA, most of the newly synthesized phage DNA made during pulses with (3)H-thymidine, and other cell constituents, and has a sedimentation rate in neutral sucrose gradients of at least 1,000S. The complex is one of the intermediates, intermediate I, in the synthesis and maturation of phage P22 DNA after infection or induction. Evidence supporting the replicative nature of intermediate I is presented. Phage replication is repressed in lysogenic bacteria. On superinfection of P22 lysogens with nonvirulent phage, little association of the input phage DNA with a rapidly sedimenting fraction is demonstrable. However, after induction with ultraviolet light, the superinfecting parental phage DNA quickly acquires the rapid sedimentation rate characteristic of intermediate I; phage DNA synthesis follows; and progeny phages are produced. Infection with a virulent mutant of P22 produces progeny phages in lysogens. Its DNA associates with intermediate I. In mixed infection with the virulent phage, replication of nonvirulent phage P22 is still repressed, even though the virulent replicates normally. The nonvirulent input DNA does not associate with intermediate I. The repressor of the lysogenic cell prevents replication by interfering with the physical association of template material with intermediate I. A phage function is required for association of phage template with the replication machinery.

Centrifugation, Density Gradient↗