RAD Genes (in Yeast)

2001 ◽  
pp. 1599
Keyword(s):  
Rad Genes

scholarly journals Characterization of mutations that suppress the temperature-sensitive growth of the hpr1 delta mutant of Saccharomyces cerevisiae.

Genetics ◽  
1994 ◽  
Vol 137 (4) ◽  
pp. 945-956 ◽  
Author(s):  
H Y Fan ◽  
H L Klein
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Synthetic Lethality ◽  
Direct Repeat ◽  
Fold Increase ◽  
Temperature Sensitive ◽  
Rad Genes ◽  
Complementation Groups ◽  
Rad Mutants ◽  
Extragenic Suppressors

Abstract The hpr1 delta 3 mutant of Saccharomyces cerevisiae is temperature-sensitive for growth at 37 degrees and has a 1000-fold increase in deletion of tandem direct repeats. The hyperrecombination phenotype, measured by deletion of a leu2 direct repeat, is partially dependent on the RAD1 and RAD52 gene products, but mutations in these RAD genes do not suppress the temperature-sensitive growth phenotype. Extragenic suppressors of the temperature-sensitive growth have been isolated and characterized. The 14 soh (suppressor of hpr1) mutants recovered represent eight complementation groups, with both dominant and recessive soh alleles. Some of the soh mutants suppress hpr1 hyperrecombination and are distinct from the rad mutants that suppress hpr1 hyperrecombination. Comparisons between the SOH genes and the RAD genes are presented as well as the requirement of RAD genes for the Soh phenotypes. Double soh mutants have been analyzed and reveal three classes of interactions: epistatic suppression of hpr1 hyperrecombination, synergistic suppression of hpr1 hyperrecombination and synthetic lethality. The SOH1 gene has been cloned and sequenced. The null allele is 10-fold increased for recombination as measured by deletion of a leu2 direct repeat.

scholarly journals Efficient isolation and mapping of rad genes of the fungus Coprinus cinereus using chromosome-specific libraries

1992 ◽  
Vol 20 (15) ◽  
pp. 3993-3997 ◽  
Author(s):  
Miriam E. Zolan ◽  
Jill R. Crittenden ◽  
Nancy K. Heyler ◽  
Lisa C. Seitz
Keyword(s):  
Coprinus Cinereus ◽  
Rad Genes

DNA structure-dependent requirements for yeast RAD genes in gene conversion

Nature ◽  
1995 ◽  
Vol 373 (6509) ◽  
pp. 84-86 ◽  
Author(s):  
N. Sugawara ◽  
E. L. Ivanov ◽  
J. Fishman-Lobell ◽  
B. L. Ray ◽  
X. Wu ◽  
...  
Keyword(s):  
Gene Conversion ◽  
Dna Structure ◽  
Rad Genes

scholarly journals THE ROLE OF RADIATION (rad) GENES IN MEIOTIC RECOMBINATION IN YEAST

Genetics ◽  
1980 ◽  
Vol 94 (1) ◽  
pp. 51-68
Author(s):  
J C Game ◽  
T J Zamb ◽  
R J Braun ◽  
M Resnick ◽  
R M Roth
Keyword(s):  
Dna Replication ◽  
Dna Synthesis ◽  
Gene Conversion ◽  
Mitotic Cell ◽  
Intragenic Recombination ◽  
Cell Cycles ◽  
Normal Functions ◽  
Rad Genes ◽  
Radiation Repair

ABSTRACT In yeast, the functions controlled by radiation-repair genes RAD6, RAD50, RAD52 and RAD57 are essential for normal meiosis; diploids with lesions in these genes either fail to sporulate (rad6) or sporulate but produce inviable spores (rad50, 52, 57). Since RAD genes may control aspects of DNA metabolism, we attempted to define more precisely the role of each gene in meiosis, especially with regard to possible roles in premeiotic DNA replication and recombination. We constructed diploids singly homozygous for each of the four rad mutations, heteroallelic at his1 and heterozygous for a recessive canavanine-resistance marker. Each strain was exposed to sporulation-inducing conditions and monitored for (1) completion of mitotic cell cycles, (2) cell viability, (3)utilization of acetate for mass increases, (4)premeiotic DNA synthesis, (5) intragenic recombination at his1, and (6) formation of viable haploid spores. Control strains heterozygous for the rad mutations completed mitosis, metabolized acetate, replicated their DNA, and showed typically high levels of gene conversion and viable-spore formation. The mutant diploids also completed mitosis, utilized acetate, and carried out premeiotic DNA replication. The mutants, however, showed little or no meiotic gene conversion. The rad50, 52 and 57 strains sporulated, but the spores were inviable. The rad6 strain did not sporulate. The rad50, 52 and 57 strains exhibited viability losses that co-incided with the period of DNA synthesis, but not with later meiotic events; the rad6 strain did not lose viability. We propose that the normal functions specified by RAD50,52 and 57 are not essential for either the initial or terminal steps in meiosis, but are required for successful recombination. The rad6 strain may be recombination-defective, o r it may fail to progress past DNA replication in the overall sequence leading to formation and recovery of meiotic recombinants.

scholarly journals RELATIONSHIPS BETWEEN A HYPER-REC MUTATION (rem1) AND OTHER RECOMBINATION AND REPAIR GENES IN YEAST

Genetics ◽  
1984 ◽  
Vol 107 (1) ◽  
pp. 33-48
Author(s):  
Robert E Malone ◽  
Merl F Hoekstra
Keyword(s):  
Meiotic Recombination ◽  
Mitotic Recombination ◽  
Repair System ◽  
X Rays ◽  
Recombination System ◽  
Damage Repair ◽  
Rad6 Gene ◽  
Recombination Repair ◽  
Rad Genes ◽  
Repair Genes

ABSTRACT Mutations in the REM1 gene of Saccharomyces cerevisiae confer a semidominant hyper-recombination and hypermutable phenotype upon mitotic cells (Golin and Esposito 1977). These effects have not been observed in meiosis. We have examined the interactions of rem1 mutations with rad6-1, rad50-1, rad52-1 or spo11-1 mutations in order to understand the basis of the rem1 hyper-rec phenotype. The rad mutations have pleiotropic phenotypes; spo11 is only defective in sporulation and meiosis. The RAD6, RAD50 and SPO11 genes are not required for spontaneous mitotic recombination; mutations in the RAD52 gene cause a general spontaneous mitotic Rec- phenotype. Mutations in RAD50, RAD52 or SPO11 eliminate meiotic recombination, and mutations in RAD6 prevent spore formation. Evidence for the involvement of RAD6 in meiotic recombination is less clear. Mutations in all three RAD genes confer sensitivity to X rays; the RAD6 gene is also required for UV damage repair. To test whether any of these functions might be involved in the hyper-rec phenotype conferred by rem1 mutations, double mutants were constructed. Double mutants of rem1 spo11 were viable and demonstrated rem1 levels of mitotic recombination, suggesting that the normal meiotic recombination system is not involved in producing the rem1 phenotype. The rem1 rad6 double mutant was also viable and had rem1 levels of mitotic recombination. Neither rem1 rad50 nor rem1 rad52 double mutants were viable. This suggests that rem1 causes its hyper-rec phenotype because it creates lesions in the DNA that are repaired using a recombination-repair system involving RAD50 and RAD52.

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