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P J Zamenhof

Publications and source records attributed to P J Zamenhof.

13 recordsLinked to original sources
PubMed1975

Molecular basis of beta-galactosidase alpha-complementation.

In previous studies, a cyanogen bromide peptide derived from amino-acid residues 3-92 of beta-galactosidase (EC 3.2.1.23; beta-D-galactoside galactohydrolase) was shown to have alpha-donor activity in intracistronic alpha-complementation. We have now isolated the defective beta-galactosidase alpha-acceptor protein from the deletion mutant strain M15 of Escherichia coli and find that it lacks residues 11-41 of betal-galactosidase. This is demonstrated by the isolation and sequence determination of a cyanogen bromide peptide from the M15 protein, which is identical to the corresponding peptide from beta-galactosidase except for the missing amino acids. We conclude that the alpha-donor peptide restores the region missing in the M15 protein.

Amino Acid Sequence↗
PubMed1975

Participation of exogenous thymine and thymidine in deoxyribonucleic acid synthesis in Lactobacillus acidophilus.

The degree of participation (DP) of exogenous thymidine and thymine in overall DNA synthesis was studied in Lactobacillus acidophilus R-26. The DP of thymidine remains constant under a variety of conditions (except at low thymidine concentrations, when the DP is influenced by deoxyribonucleosides and folic acid). A 5-bromodeoxyuridine-resistant mutant was isolated, which displayed cross-resistance to 5-bromouracil and a significantly lower DP of thymidine than the parental strain. Thymine was poorly incorporated in the parental strain even in the presence of deoxyribosides. The results of this investigation would be compatible with the possibility of an alternative pathway for thymidylate synthesis other than the known thymidylate synthase pathway.

Bromodeoxyuridine↗
PubMed1974

Degradation of thymidine by Lactobacillus acidophilus.

Whole cells of Lactobacillus acidophilus are capable of degrading thymidine to thymine, suggesting the presence of thymidine phosphorylase (or thymidine hydrolase). This activity was also demonstrated in cell-free extracts.

Arsenic↗
PubMed1972

Construction and properties of Escherichia coli strains exhibiting -complementation of -galactosidase fragments in vivo.

In vivo alpha-complementation of beta-galactosidase was demonstrated in 16 Z gene terminator (nonsense) mutant strains of Escherichia coli upon introduction of the episome F'M15 which specifies production of a mutant Z gene polypeptide containing a small deletion in the N-terminal region of the enzyme monomer. Genetic and biochemical analyses of the merodiploids showed that restoration of enzyme activity was due to their terminator/F'M15 genetic constitution resulting in the production of two enzymatically inactive polypeptides which associate in vivo to reconstitute active, stable beta-galactosidase. The prematurely terminated polypeptide fragments known to be rapidly degraded in haploid cells were shown by phenotypic and biochemical studies to be stabilized (i.e., protected) in merodiploids by formation of complemented enzyme complexes with the M15 protein. Phenotypic properties of complementing diploids are described and are discussed in relation to in vitro determination of beta-galactosidase activity.

Coliphages↗
PubMed1965

Genetic Factors in Radiation Resistance of Bacillus subtilis.

Zamenhof, Stephen (University of California, Los Angeles), Hela Bursztyn, T. K. Ramachandra Reddy, and Patrice J. Zamenhof. Genetic factors in radiation resistance of Bacillus subtilis. J. Bacteriol. 90:108-115. 1965.-A study of several wild cross-transformable strains of Bacillus subtilis revealed differences in the resistance of their spores to X rays. Closer study of two such strains revealed differences of the same type when vegetative cells were exposed to X rays or to ultraviolet light (UV). Cell cultures repeatedly exposed to sublethal doses of UV (with cultivation between exposures) became more resistant to UV, presumably by enrichment in a more UV-resistant mutant. A sulfanilamide-resistant mutant of one strain (vegetative cells and spores) was less resistant to ionizing radiation; this sensitivity was transferable by transformation. No difference in radiation-induced mutability could be demonstrated in any of the strains studied. It is concluded that, at least in the cases studied, (i) the differences in radiation resistance of spores of different strains are not just a result of a superimposition of a common spore resistance mechanism(s) but rather are an amplification of genetically determined resistance differences in vegetative cells of these strains; (ii) sulfanilamide-resistance locus (p-aminobenzoic acid overproduction locus) is one of the loci of radiation sensitivity; (iii) no evidence was obtained that the differences in radiation resistance of cells or spores can be ascribed to differences in radiation resistance of their deoxyribonucleic acid.

Journal Article↗