The influence of defects in excision and error prone repair on spontaneous and induced mitotic recombination and mutation in Saccharomyces cerevisiae

1978 ◽  
Vol 161 (1) ◽  
pp. 81-88 ◽  
Author(s):  
R. Kern ◽  
F. K. Zimmermann
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitotic Recombination ◽  
Error Prone Repair

scholarly journals Regulation of Mitotic Homeologous Recombination in Yeast: Functions of Mismatch Repair and Nucleotide Excision Repair Genes

Genetics ◽  
2000 ◽  
Vol 154 (1) ◽  
pp. 133-146 ◽  
Author(s):  
Ainsley Nicholson ◽  
Miyono Hendrix ◽  
Sue Jinks-Robertson ◽  
Gray F Crouse
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mismatch Repair ◽  
Nucleotide Excision Repair ◽  
Excision Repair ◽  
Mitotic Recombination ◽  
Inverted Repeats ◽  
Replication Errors ◽  
Nucleotide Excision ◽  
Homeologous Recombination ◽  
Repair Genes

Abstract The Saccharomyces cerevisiae homologs of the bacterial mismatch repair proteins MutS and MutL correct replication errors and prevent recombination between homeologous (nonidentical) sequences. Previously, we demonstrated that Msh2p, Msh3p, and Pms1p regulate recombination between 91% identical inverted repeats, and here use the same substrates to show that Mlh1p and Msh6p have important antirecombination roles. In addition, substrates containing defined types of mismatches (base-base mismatches; 1-, 4-, or 12-nt insertion/deletion loops; or 18-nt palindromes) were used to examine recognition of these mismatches in mitotic recombination intermediates. Msh2p was required for recognition of all types of mismatches, whereas Msh6p recognized only base-base mismatches and 1-nt insertion/deletion loops. Msh3p was involved in recognition of the palindrome and all loops, but also had an unexpected antirecombination role when the potential heteroduplex contained only base-base mismatches. In contrast to their similar antimutator roles, Pms1p consistently inhibited recombination to a lesser degree than did Msh2p. In addition to the yeast MutS and MutL homologs, the exonuclease Exo1p and the nucleotide excision repair proteins Rad1p and Rad10p were found to have roles in inhibiting recombination between mismatched substrates.

scholarly journals INDUCTION OF MITOTIC CROSSING OVER IN SACCHAROMYCES CEREVISIAE BY BREAKDOWN PRODUCTS OF DIMETHYLNITROSAMINE, DIETHYLNITROSAMINE, 1-NAPHTHYLAMINE AND 2-NAPHTHYLAMINE FORMED BY AN IN VITRO HYDROXYLATION SYSTEM

Genetics ◽  
1973 ◽  
Vol 74 (3) ◽  
pp. 433-442
Author(s):  
V W Mayer
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitotic Recombination ◽  
Crossing Over ◽  
Genetic Damage ◽  
Nitroso Group ◽  
Damage Potential ◽  
Test Conditions

ABSTRACT Dimethylnitrosamine and diethylnitrosamine, two potent carcinogens, are nonmutagenic when tested directly in microorganisms. Likewise 1-naphthylamine and 2-naphthylamine are also nonmutagenic but the N-hydroxy derivatives are mutagenic in microorganisms. Apparently these compounds require metabolism to breakdown products which are then the proximately active agents, and microorganisms lack the enzymes necessary to effect this conversion. These compounds are mutagenic in Saccharomyces after conversion to breakdown products in an in vitro hydroxylation medium. The induction of mitotic crossing over in Saccharomyces cerevisiae by breakdown products of dimethylnitrosamine, diethylnitrosamine, 1-naphthylamine and 2-naphthylamine formed in the Udenfriend hydroxylation medium is reported in this communication. Mitotic crossing over was detected as red sectored colonies resulting from induced homozygosity of the ade2 marker. Dimethylamine and diethylamine, which lack the nitroso group of the nitrosamines, did not induce mitotic crossing over under any of the test conditions. To further confirm that the induced sectored colonies were the result of mitotic crossing over they were tested for the presence of reciprocal products. The expected reciprocal products were found in over 67% of the isolates tested. The significance and practicality of using mitotic recombination as an indicator of genetic damage potential of chemicals is discussed.

Mitotic recombination in Saccharomyces cerevisiae

2003 ◽  
Vol 42 (4) ◽  
pp. 185-198 ◽  
Author(s):  
Félix Prado ◽  
Felipe Cortés-Ledesma ◽  
Pablo Huertas ◽  
Andrés Aguilera
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mitotic Recombination

scholarly journals RAD10, an excision repair gene of Saccharomyces cerevisiae, is involved in the RAD1 pathway of mitotic recombination.

1990 ◽  
Vol 10 (6) ◽  
pp. 2485-2491 ◽  
Author(s):  
R H Schiestl ◽  
S Prakash
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Meiotic Recombination ◽  
Excision Repair ◽  
Mitotic Recombination ◽  
The Other ◽  
Gene Products ◽  
Repair Gene ◽  
Homologous Chromosomes ◽  
Intrachromosomal Recombination ◽  
Recombination Pathway

The RAD10 gene of Saccharomyces cerevisiae is required for the incision step of excision repair of UV-damaged DNA. We show that the RAD10 gene is also required for mitotic recombination. The rad10 delta mutation lowered the rate of intrachromosomal recombination of a his3 duplication in which one his3 allele has a deletion at the 3' end and the other his3 allele has a deletion at the 5' end (his3 delta 3' his3 delta 5'). The rate of formation of HIS3+ recombinants in the rad10 delta mutant was not affected by the rad1 delta mutation but decreased synergistically in the presence of the rad10 delta mutation in combination with the rad52 delta mutation. These observations indicate that the RAD1 and RAD10 genes function together in a mitotic recombination pathway that is distinct from the RAD52 recombination pathway. The rad10 delta mutation also lowered the efficiency of integration of linear DNA molecules and circular plasmids into homologous genomic sequences. We suggest that the RAD1 and RAD10 gene products act in recombination after the formation of the recombinogenic substrate. The rad1 delta and rad10 delta mutations did not affect meiotic intrachromosomal recombination of the his3 delta 3' his3 delta 5' duplication or mitotic and meiotic recombination of ade2 heteroalleles located on homologous chromosomes.

scholarly journals Differential mismatch repair can explain the disproportionalities between physical distances and recombination frequencies of cyc1 mutations in yeast.

Genetics ◽  
1988 ◽  
Vol 119 (1) ◽  
pp. 21-34
Author(s):  
C W Moore ◽  
D M Hampsey ◽  
J F Ernst ◽  
F Sherman
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Mismatch Repair ◽  
Meiotic Recombination ◽  
Mitotic Recombination ◽  
The Other ◽  
Recombination Rates ◽  
Base Pairs ◽  
Yeast Saccharomyces Cerevisiae ◽  
X Ray ◽  
Mismatched Base Pair

Abstract Recombination rates have been examined in two-point crosses of various defined cyc1 mutations that cause the loss or nonfunction of iso-1-cytochrome c in the yeast Saccharomyces cerevisiae. Recombinants arising by three different means were investigated, including X-ray induced mitotic recombination, spontaneous mitotic recombination, and meiotic recombination. Heteroallelic diploid strains were derived by crossing cyc1 mutants containing a series of alterations at or near the same site to cyc1 mutants containing alterations at various distances. Marked disproportionalities between physical distances and recombination frequencies were observed with certain cyc1 mutations, indicating that certain mismatched bases can significantly affect recombination. The marker effects were more pronounced when the two mutational sites of the heteroalleles were within about 20 base pairs, but separated by at least 4 base pairs. Two alleles, cyc1-163 and cyc1-166, which arose by G.C----C.G transversions at nucleotide positions 3 and 194, respectively, gave rise to especially high rates of recombination. Other mutations having different substitutions at the same nucleotide positions were not associated with abnormally high recombination frequencies. We suggest that these marker effects are due to the lack of repair of either G/G or C/C mismatched base pairs, while the other mismatched base pair of the heteroallele undergoes substantial repair. Furthermore, we suggest that diminished recombination frequencies are due to the concomitant repair of both mismatches within the same DNA tract.

RAD52-INDEPENDENT MITOTIC GENE CONVERSION IN SACCHAROMYCES CEREVISIAE FREQUENTLY RESULTS IN CHROMOSOMAL LOSS

Genetics ◽  
1985 ◽  
Vol 111 (1) ◽  
pp. 7-22
Author(s):  
James E Haber ◽  
Mark Hearn
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Gene Conversion ◽  
Mitotic Recombination ◽  
Gene Conversion Event ◽  
Intragenic Recombination ◽  
Wild Type ◽  
Conversion Event ◽  
Chromosomal Loss ◽  
Mitotic Gene Conversion ◽  
Striking Effect

ABSTRACT We have examined spontaneous, interchromosomal mitotic recombination events between his4 alleles in both Rad+ and rad52 strains of Saccharomyces cerevisiae. In Rad+ strains, 74% of the His+ prototrophs resulted from gene conversion events without exchange of flanking markers. In diploids homozygous for the rad52-1 mutation, the frequency of His+ prototroph formation was less than 5% of the wild-type value, and more than 80% of the gene conversion events were accompanied by an exchange of flanking markers. Most of the rad52 intragenic recombination events arose by gene conversion accompanied by an exchange of flanking markers and not by a simple reciprocal exchange between the his4A and his4C alleles. There were also profound effects on the kinds of recombinant products that were recovered. The most striking effect was that RAD52-independent mitotic recombination frequently results in the loss of one of the two chromosomes participating in the gene conversion event.

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