Postmeiotic Segregation Increased 2: PMS2

Genetics ◽  
1996 ◽  
Vol 142 (2) ◽  
pp. 407-416 ◽  
Author(s):  
P Manivasakam ◽  
Susan M Rosenberg ◽  
P J Hastings

Abstract In yeast meiotic recombination, alleles used as genetic markers fall into two classes as regards their fate when incorporated into heteroduplex DNA. Normal alleles are those that form heteroduplexes that are nearly always recognized and corrected by the mismatch repair system operating in meiosis. High PMS (postmeiotic segregation) alleles form heteroduplexes that are inefficiently mismatch repaired. We report that placing any of several high PMS alleles very close to normal alleles causes hyperrecombination between these markers. We propose that this hyperrecombination is caused by the high PMS allele blocking a mismatch repair tract initiated from the normal allele, thus preventing corepair of the two alleles, which would prevent formation of recombinants. The results of three point crosses involving two PMS alleles and a normal allele suggest that high PMS alleles placed between two alleles that are normally corepaired block that corepair.


Genetics ◽  
1988 ◽  
Vol 119 (2) ◽  
pp. 329-336
Author(s):  
T Langin ◽  
H Hamza ◽  
V Haedens ◽  
J L Rossignol

Abstract In the gene b2 of Ascobolus immersus, large heterologies increase the frequencies of reciprocal exchanges on their upstream border (corresponding to the high non-Mendelian segregation side). Tests were made to determine whether these reciprocal exchanges, instigated by large heterologies, resulted from the blockage of a Holliday junction bordering a hybrid DNA tract extending from the end of the gene to the heterology. Three types of experiments were performed to answer this question. In all cases, results did not correlate the presence of reciprocal exchanges instigated by large heterologies with the presence of adjacent hybrid DNA tracts. These reciprocal exchanges were rarely associated with postmeiotic segregation at upstream markers, they were not associated with gene conversion of a marker within the interval and their frequency was not decreased by decreasing the frequency of hybrid DNA formation in the gene. These results led to the proposal of the existence of a precursor to reciprocal exchange different from a single branch-migrating Holliday junction. This precursor migrates rightward and its migration is dependent on the DNA sequence homology. The existence of this precursor does not exclude that reciprocal exchanges resulting from the maturation of single Holliday junctions bordering adjacent hybrid DNA tracts could also occur.


1977 ◽  
Vol 30 (3) ◽  
pp. 308-308

The detection, in unordered octads, of 6+:2m and 2+:6m ratios with postmeiotic segregation, and of aberrant 4:4s and their use in corresponding-site interference studiesBY AGLAIA GHIKAS AND B. C. LAMBDepartment of Botany, Imperial College, London SWl 2BBVol. 29, No. 3 p. 273.The first line should read ‘originally PD or NPD 4:4(4)s,’.Sterile mutation in Drosophila melanogasterBY TAKAO K. WATANABE AND WON HO LEENational Institute of Genetics, Mishima 411, JapanVol. 30, No. 2.p. 110, second line: for ‘Avery Period’ read ‘P. J. Avery’.p. 111, 4 lines from foot of page: formula should readp. 112, line 4: start of line should readThe contribution of plasmid and host genes to plasmid-mediated interference with phage growthBY VICTORIA HUGHES AND G. G. MEYNELLBiological Laboratory, University of Kent, Canterbury, Kent CT2 4tNJ, EnglandVol. 30, No. 2.p. 180, line 12: ‘2000μg streptomycin’ should read ‘200μg streptomycin’.The basis for an apparent auxotrophy for reduced sulphur metabolites in sF−mutants of Aspergillus nidulansBY HERBERT N. ARTS, JR.Department of Genetics, University of Cambridge, Downing Street, Cambridge CB2 3EH, EnglandVol. 30, No. 2.p. 209, note added in proof line 9: ‘does not protect sF-211 strains’ should read ‘does protect sF-211 strains’.


1981 ◽  
Vol 38 (3) ◽  
pp. 281-296 ◽  
Author(s):  
Arthur J. Hilliker ◽  
Arthur Chovnick

SUMMARYThis report examines several issues bearing upon intragenic recombination in higher eukaryotes. The fine structure data accumulated in our analysis of the genetic organization of the rosy locus in Drosophila melanogaster. Firstly, we confirm that a conversion event has a markedly less than 50% probability of resulting in flanking marker exchange, a finding consistent with more recent analyses of the available Saccharomyces data (e.g. Fogel et al. 1978). As reported earlier, co-conversion of recombinationally separable sites within the rosy locus occurs (McCarron, Gelbart & Chovnick, 1974). In this report, we demonstrate that the frequency of co-conversion is inversely proportional to the distance between co-converting sites. As in fungi, real conversion frequency differences are observed among rosy mutant alleles, and the data suggest that there may be a relationship between allele conversion frequency and map position. Unlike Neurospora and Saccharomyces, only one flanking marker exchange class is recovered from any given mutant heteroallele recombination experiment. In this respect, the Drosophila system resembles Aspergillus. As in Neurospora and Saccharomyces, rosy locus intragenic recombinants associated with flanking marker exchange exhibit interference with crossing over in adjacent regions, while no interference is seen among recombinants exhibiting parental flanking markers. Finally, experimental results are discussed which demonstrate the occurrence of postmeiotic segregation in Drosophila. These analogies between Drosophila and fungi provide further evidence in support of the notion that eukaryotes share common molecular mechanism(s) of meiotic recombination.


2003 ◽  
Vol 23 (3) ◽  
pp. 873-886 ◽  
Author(s):  
Juan Lucas Argueso ◽  
Amanda Wraith Kijas ◽  
Sumeet Sarin ◽  
Julie Heck ◽  
Marc Waase ◽  
...  

ABSTRACT In eukaryotic cells, DNA mismatch repair is initiated by a conserved family of MutS (Msh) and MutL (Mlh) homolog proteins. Mlh1 is unique among Mlh proteins because it is required in mismatch repair and for wild-type levels of crossing over during meiosis. In this study, 60 new alleles of MLH1 were examined for defects in vegetative and meiotic mismatch repair as well as in meiotic crossing over. Four alleles predicted to disrupt the Mlh1p ATPase activity conferred defects in all functions assayed. Three mutations, mlh1-2, -29, and -31, caused defects in mismatch repair during vegetative growth but allowed nearly wild-type levels of meiotic crossing over and spore viability. Surprisingly, these mutants did not accumulate high levels of postmeiotic segregation at the ARG4 recombination hotspot. In biochemical assays, Pms1p failed to copurify with mlh1-2, and two-hybrid studies indicated that this allele did not interact with Pms1p and Mlh3p but maintained wild-type interactions with Exo1p and Sgs1p. mlh1-29 and mlh1-31 did not alter the ability of Mlh1p-Pms1p to form a ternary complex with a mismatch substrate and Msh2p-Msh6p, suggesting that the region mutated in these alleles could be responsible for signaling events that take place after ternary complex formation. These results indicate that mismatches formed during genetic recombination are processed differently than during replication and that, compared to mismatch repair functions, the meiotic crossing-over role of MLH1 appears to be more resistant to mutagenesis, perhaps indicating a structural role for Mlh1p during crossing over.


1988 ◽  
Vol 8 (3) ◽  
pp. 1253-1258 ◽  
Author(s):  
J H White ◽  
J F DiMartino ◽  
R W Anderson ◽  
K Lusnak ◽  
D Hilbert ◽  
...  

The meiotic behavior of two graded series of deletion mutations in the ADE8 gene in Saccharomyces cerevisiae was analyzed to investigate the molecular basis of meiotic recombination. Postmeiotic segregation (PMS) was observed for a subset of the deletion heterozygosities, including deletions of 38 to 93 base pairs. There was no clear relationship between deletion length and PMS frequency. A common sequence characterized the novel joint region in the alleles which displayed PMS. This sequence is related to repeated sequences recently identified in association with recombination hotspots in the human and mouse genomes. We propose that these particular deletion heterozygosities escape heteroduplex DNA repair because of fortuitous homology to a binding site for a protein.


1999 ◽  
Vol 19 (1) ◽  
pp. 241-250 ◽  
Author(s):  
Claudia Rudolph ◽  
Christophe Kunz ◽  
Sandro Parisi ◽  
Elisabeth Lehmann ◽  
Edgar Hartsuiker ◽  
...  

ABSTRACT We have identified in the fission yeast Schizosaccharomyces pombe a MutS homolog that shows highest homology to the Msh2 subgroup. msh2 disruption gives rise to increased mitotic mutation rates and increased levels of postmeiotic segregation of genetic markers. In bandshift assays performed with msh2Δ cell extracts, a general mismatch-binding activity is absent. By complementation assays, we showed that S. pombe msh2 is allelic with the previously identified swi8 andmut3 genes, which are involved in mating-type switching. The swi8-137 mutant has a mutation in the msh2gene which causes a truncated Msh2 peptide lacking a putative DNA-binding domain. Cytological analysis revealed that during meiotic prophase of msh2-defective cells, chromosomal structures were frequently formed; such structures are rarely found in the wild type. Our data show that besides having a function in mismatch repair,S. pombe msh2 is required for correct termination of copy synthesis during mating-type switching as well as for proper organization of chromosomes during meiosis.


1988 ◽  
Vol 8 (3) ◽  
pp. 1253-1258
Author(s):  
J H White ◽  
J F DiMartino ◽  
R W Anderson ◽  
K Lusnak ◽  
D Hilbert ◽  
...  

The meiotic behavior of two graded series of deletion mutations in the ADE8 gene in Saccharomyces cerevisiae was analyzed to investigate the molecular basis of meiotic recombination. Postmeiotic segregation (PMS) was observed for a subset of the deletion heterozygosities, including deletions of 38 to 93 base pairs. There was no clear relationship between deletion length and PMS frequency. A common sequence characterized the novel joint region in the alleles which displayed PMS. This sequence is related to repeated sequences recently identified in association with recombination hotspots in the human and mouse genomes. We propose that these particular deletion heterozygosities escape heteroduplex DNA repair because of fortuitous homology to a binding site for a protein.


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