Mitotic intragenic recombination in the yeast Saccharomyces: marker-effects on conversion and reciprocity of recombination

Chernoff, Yury O.; Kidgotko, O. V.; Demberelijn, O.; Luchnikova, I. L.; Soldatov, S. P.; Глазер, В.М.; Gordenin, Dmitry A.

doi:10.1007/bf00396201

Cited by 11 publications

(5 citation statements)

References 19 publications

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“…Available evidence indicates that heteroduplex extension through a region this size should not present an obstacle for the yeast recombination machinery. Mitotic gene conversion of lys2 deletions in the 1-to 2-kb range has been reported (8), as well as conversion of a 6-kb Ty element inserted within the URA3 locus (50).…”

Section: Discussionmentioning

confidence: 99%

Mismatch Repair Proteins Regulate Heteroduplex Formation during Mitotic Recombination in Yeast

Chen

Jinks-Robertson

1998

Molecular and Cellular Biology

105

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Mismatch repair (MMR) proteins actively inhibit recombination between diverged sequences in both prokaryotes and eukaryotes. Although the molecular basis of the antirecombination activity exerted by MMR proteins is unclear, it presumably involves the recognition of mismatches present in heteroduplex recombination intermediates. This recognition could be exerted during the initial stage of strand exchange, during the extension of heteroduplex DNA, or during the resolution of recombination intermediates. We previously used an assay system based on 350-bp inverted-repeat substrates to demonstrate that MMR proteins strongly inhibit mitotic recombination between diverged sequences in Saccharomyces cerevisiae. The assay system detects only those events that reverse the orientation of the region between the recombination substrates, which can occur as a result of either intrachromatid crossover or sister chromatid conversion. In the present study we sequenced the products of mitotic recombination between 94%-identical substrates in order to map gene conversion tracts in wild-type versus MMR-defective yeast strains. The sequence data indicate that (i) most recombination occurs via sister chromatid conversion and (ii) gene conversion tracts in an MMR-defective strain are significantly longer than those in an isogenic wild-type strain. The shortening of conversion tracts observed in a wild-type strain relative to an MMR-defective strain suggests that at least part of the antirecombination activity of MMR proteins derives from the blockage of heteroduplex extension in the presence of mismatches.Homologous recombination events can be either reciprocal or nonreciprocal in nature. Reciprocal recombination (crossing over) alters the linkage relationships of loci that flank the site of an exchange, whereas nonreciprocal recombination (gene conversion) is defined as the unidirectional transfer of information from one DNA molecule to another. All present models of recombination stipulate the formation of a heteroduplex recombination intermediate, which is formed by complementary base pairing of single strands derived from different duplexes. Correction of a mismatch in heteroduplex DNA can result in a gene conversion event, and such correction is effected by the same mismatch repair (MMR) machinery that corrects errors made during DNA replication. Cocorrection of a series of contiguous mismatches generates a conversion tract, the length of which is considered to be a minimal estimate of the extent of the heteroduplex intermediate formed. The point at which the recombining molecules exchange single strands to form heteroduplex DNA is referred to as a Holliday junction, and cleavage of this junction gives rise to crossovers and noncrossovers at roughly equivalent frequencies.Homologous recombination usually involves allelic sequences on homologous chromosomes but also can occur between dispersed (ectopic) repeated sequences. Ectopic gene conversion provides a mechanism for homogenizing repeated sequences and hence is important in t...

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Section: Discussionmentioning

confidence: 99%

Mismatch Repair Proteins Regulate Heteroduplex Formation during Mitotic Recombination in Yeast

Chen

Jinks-Robertson

1998

Molecular and Cellular Biology

105

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“…We and others (9, 32) have demonstrated with several heteroallelic pairs of mutations in the LYS2, URA3, HIS4, and HIS3 genes that a large insertion (as well as deletions) can lead to as much as a 19-fold bias in favor of loss of a point mutation; this is in contrast to the present findings involving the TnS insertion. (The only exception was iys2-32 [9]; however, this mutation was subsequently shown to be due to a large Tyl insertion [8].) The absence of conversion bias for the heteroallelic pairs of point mutations that do not exhibit hotspots is well documented (28).…”

Section: Discussionmentioning

confidence: 99%

Inverted DNA repeats: a source of eukaryotic genomic instability.

Gordenin¹,

Lobachev²,

Degtyareva³

et al. 1993

Mol. Cell. Biol.

143

136

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While inverted DNA repeats are generally acknowledged to be an important source of genetic instability in prokaryotes, relatively little is known about their effects in eukaryotes. Using bacterial transposon Tn5 and its derivatives, we demonstrate that long inverted repeats also cause genetic instability leading to deletion in the yeast Saccharomyces cerevisiae. Furthermore, they induce homologous recombination. Replication plays a major role in the deletion formation. Deletions are stimulated by a mutation in the DNA polymerase delta gene (pol3). The majority of deletions result from imprecise excision between small (4- to 6-bp) repeats in a polar fashion, and they often generate quasipalindrome structures that subsequently may be highly unstable. Breakpoints are clustered near the ends of the long inverted repeats (< 150 bp). The repeats have both intra- and interchromosomal effects in that they also create hot spots for mitotic interchromosomal recombination. Intragenic recombination is 4 to 18 times more frequent for heteroalleles in which one of the two mutations is due to the insertion of a long inverted repeat, compared with other pairs of heteroalleles in which neither mutation has a long repeat. We propose that both deletion and recombination are the result of altered replication at the basal part of the stem formed by the inverted repeats.

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“…recombinational marker-effects of deletions and Tyl insertion (Chernoff et al, 1984;Chernoff and Gordenin, 1987) and on the conversion of Tn5 insertions is under investigation.…”

Section: Discussionmentioning

confidence: 99%

Yeast mutants with increased bacterial transposon Tn5 excision

Gordenin

Proscyavichus²,

Malkova

et al. 1991

Yeast

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Five complementing recessive mutations that exhibit increased bacterial transposon Tn5 precise excision in yeast Saccharomyces cerevisiae were obtained by ethylmethanesulfonate treatment. One of these mutations (tex1) was submitted to extensive genetic analysis. tex1 is a recessive temperature-sensitive mutation resulting in a 20-100-fold increase in Tn5 excision. It also has increased frequencies of ochre mutation reversion, of forward mutation to canavanine resistance, and loss of chromosome III or its right arm. The possible mechanism of tex1 effects is discussed.

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Mitotic intragenic recombination in the yeast Saccharomyces: marker-effects on conversion and reciprocity of recombination

Cited by 11 publications

References 19 publications

Mismatch Repair Proteins Regulate Heteroduplex Formation during Mitotic Recombination in Yeast

Mismatch Repair Proteins Regulate Heteroduplex Formation during Mitotic Recombination in Yeast

Inverted DNA repeats: a source of eukaryotic genomic instability.

Yeast mutants with increased bacterial transposon Tn5 excision

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