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Biomedical subjects

M A Resnick

Publications and source records attributed to M A Resnick.

108 records · Page 6Linked to original sources
PubMed1977

Nuclear DNA synthesis in yeast and the effect of irradiation.

The synthesis of DNA can be measured in yeast by following the uptake of 5-bromodeoxy-uridine-5'-triphosphate in a mutant that utilizes deoxythymidine-5'-monophosphate; approximately 60 per cent of the DNA is synthesized semi-conservatively before replication stops. Neither ultraviolet light (U.V.), nor ionizing radiation stimulates repair-type synthesis. Based on the ability to detect small amounts of synthesis, it appears that fewer than ten bases are synthesized per pyrimidine dimer removed.

Cell Nucleus↗
PubMed1976

The repair of double-strand breaks in the nuclear DNA of Saccharomyces cerevisiae and its genetic control.

With the use of neutral sucrose sedimentation techniques, the size of unirradiated nuclear DNA and the repair of double-strand breaks induced in it by ionizing radiation have been determined in both wild-type and homozygous rad52 diploids of the yeast Saccharomyces cerevisiae. The number average molecular weight of unirradiated DNA in these experiments is 3.0 X 10(8)+/-0.3 Daltons. Double-strand breaks are induced with a frequency of 0.58 X 10(-10) per Daltonkrad in the range of 25 to 100 krad. Since repair at low doses is observed in wild-type but not homozygous rad52 strains, the corresponding rad52 gene product is concluded to have a role in the repair process. Cycloheximide was also observed to inhibit repair to a limited extent indicating a requirement for protein synthesis. Based on the sensitivity of various mutants and the induction frequency of double-strand breaks, it is concluded that there are 1 to 2 double-strand breaks per lethal event in diploid cells incapable of repairing these breaks.

Centrifugation, Density Gradient↗
PubMed1975

The repair of double-strand breaks in chromosomal DNA of yeast.

Ionizing radiation induces double-strand breaks in the nuclear DNA of the yeast Saccharomyces cerevisiae with an efficiency of approximately 0.6 X 10(-10) breaks being repaired. Based on the efficiency of break production, the sensitivity of a rad52 mutant, and the absence of radiation-induced recombination in such a mutant, it is proposed that the corresponding gene product may be involved in double-strand break repair. A model involving recombination and DNA synthesis is described for this type of repair.

Chromosomes↗
PubMed1972

Photoreactivation and gene dosage in yeast.

The amount of photoreactivating enzyme in tetraploid cells of Saccharomyces cerevisiae and the ability of the cells to be photoreactivated after ultraviolet irradiation are directly proportional to the number of genes per cell involved in the synthesis of photoreactivating enzyme.

Bacteriological Techniques↗
PubMed1972

Repair of pyrimidine dimer damage induced in yeast by ultraviolet light.

Crude extracts from ultraviolet (UV)-irradiated yeast cells compete with UV-irradiated transforming deoxyribonucleic acid (DNA) for photoreactivating enzyme. The amount of competition is taken as a measure of the level of cyclobutyl pyrimidine dimers in the yeast DNA. A calibration of the competition using UV-irradiated calf thymus DNA indicates that an incident UV dose (1,500 ergs/mm(2)) yielding 1% survivors of wild-type cells produces between 2.5 x 10(4) to 5 x 10(4) dimers per cell. Wild-type cells irradiated in the exponential phase of growth remove or alter more than 90% of the dimers within 220 min after irradiation. Pyrimidine dimers induced in stationary-phase wild-type cells appear to remain in the DNA; however, with incubation, they become less photoreactivable in vivo, although remaining photoreactivable in vitro. In contrast, exponentially growing or stationary-phase UV-sensitive cells (rad2-17) show almost no detectable alteration of dimers. We conclude that the UV-sensitive cells lack an early step in the repair of UV-induced pyrimidine dimers.

Animals↗
PubMed1966

Unsaturated fatty acid mutants of Saccharomyces cerevisiae.

Resnick, Michael A. (University of California, Berkeley), and Robert K. Mortimer. Unsaturated fatty acid mutants of Saccharomyces cerevisiae. J. Bacteriol. 92:597-600. 1966.-The wild type of the yeast Saccharomyces cerevisiae does not require fatty acids or sterols for growth. Two types of lipid nutritional mutants have been induced in this organism. One of these classes of mutants requires an unsaturated fatty acid and is associated with a locus on chromosome VII. The other class of mutants needs either an unsaturated fatty acid or ergosterol for growth. Experiments involving identification and characterization of these mutants are presented.

Chromosome Mapping↗
PubMedDate not supplied

Genetic change may be caused by interference with protein-protein interactions.

Several aprotic polar solvents were shown to induce mitotic aneuploidy in yeast: diethyl ketone, gamma-valerolactone, pyridine, pivalinic acid nitrile, phenylacetonitrile and fumaric acid dinitrile. Only fumaric acid dinitrile also strongly induced other types of genetic effects including mitotic crossing-over, mitotic gene conversion and point mutation. The other substances only induced aneuploidy and this only over a very narrow dose range. The treatment protocol used suggested that these chemicals acted via interference with tubulin assembly and disassembly causing a malfunctioning of spindle fiber microtubules. This hypothesis was tested using twice recycled porcine brain tubulin. Diethyl ketone, gamma-valerolactone, pyridine and phenylacetonitrile inhibited GTP-promoted assembly of porcine brain tubulin in vitro in the concentration range needed for the induction of mitotic aneuploidy in yeast. Pivalinic acid nitrile accelerated tubulin aggregation whereas fumaric acid dinitrile had no effect even at concentrations 18 times higher than the lowest tested concentration effective in yeast. The in vitro experiments with porcine brain tubulin further suggest that genetic change can result from interference with specific protein-protein interactions. Fumaric acid dinitrile was the only exception since it did induce aneuploidy but had no effects on the assembly of porcine brain tubulin. This could be caused either by interference with protein-protein interactions other than between molecules during assembly and disassembly of microtubules or species-specific differences in susceptibility between yeast spindle and porcine brain tubulin.

Aneuploidy↗
PubMedDate not supplied

The detection of chemically induced aneuploidy in Saccharomyces cerevisiae: an assessment of mitotic and meiotic systems.

Several systems have been evaluated for their ability to detect aneuploidy. Chromosome gain can be detected in mitotic haploid cells as well as meiotically derived haploid spores. Both chromosome gain and loss are detectable in mitotic diploid cells. Several chemicals have been identified that clearly induce aneuploidy in at least one or more of the systems.

Aneuploidy↗