Characterization of <i>REC104</i>, a gene required for early meiotic recombination in the yeast <i>Saccharomyces cerevisiae</i>

Galbraith, Anne M.; Malone, Robert E.

doi:10.1002/dvg.1020130603

Cited by 27 publications

(11 citation statements)

References 37 publications

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“…We also consider it unlikely that DSBs are formed by any of the known S.cerevisiae double-strand endonucleases, since these display a high degree of sequence specificity and cleave DNA to form 3' single-strand overhangs (Kostriken et al, 1983;Dujon et al, 1989;Gimble and Thorner, 1993). Instead, we suggest that the yeast DSBforming activity may be encoded by one or more members of the set of meiosis-induced yeast genes, mutations in which confer a recombination-null phenotype (Engebrecht et al, 1991;Malone et al, 1991;Cool and Malone, 1992;Galbraith and Malone, 1992;Menees et al, 1992;Pittman et al, 1993). Implications for the mechanism and control of meiotic recombination initiation The mechanism proposed above, in that it is similar to that proposed for topoisomerase II, provides a potential way to ensure that the first step of DSB formation is reversible.…”

Section: Discussionmentioning

confidence: 85%

The location and structure of double-strand DNA breaks induced during yeast meiosis: evidence for a covalently linked DNA-protein intermediate.

1995

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We have determined the precise location and structure of the double‐strand DNA breaks (DSBs) formed during Saccharomyces cerevisiae meiosis. Breaks were examined at two recombination hot spots in both wild‐type and rad50S mutant cells. At both loci, breaks occurred at multiple, irregularly spaced sites in a approximately 150 nucleotide interval contained within an area of nuclease‐hypersensitive chromatin. No consensus sequence could be discerned at or around break sites. Patterns of cleavage observed on individual strands indicated that breaks initially form with a two nucleotide 5′ overhang. Broken strands from rad50S mutant cells contained tightly bound protein at their 5′ ends. We suggest that, in S.cerevisiae, meiotic recombination is initiated by a DSB‐forming activity that creates a covalently linked protein‐DNA intermediate.

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Section: Discussionmentioning

confidence: 85%

The location and structure of double-strand DNA breaks induced during yeast meiosis: evidence for a covalently linked DNA-protein intermediate.

1995

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“…Mutations in these ''early exchange'' genes [e.g., REC104 (18)] reduce meiotic recombination to background mitotic levels; in those that have been tested, DSBs are not detectable (e.g., see Fig. 2).…”

Section: Discussionmentioning

confidence: 99%

Double strand breaks at the HIS2 recombination hot spot in Saccharomyces cerevisiae

Bullard

Kim

Galbraith

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

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Double strand breaks (DSBs) have been found at several meiotic recombination hot spots in Saccharomyces cerevisiae; more global studies have found that they occur at many places along several yeast chromosomes during meiosis. Indeed, the number of breaks found is consistent with the number of recombination events predicted from the genetic map. We have previously demonstrated that the HIS2 gene is a recombination hot spot, exhibiting a high frequency of gene conversion and associated crossing over. This paper shows that DSBs occur in meiosis at a site in the coding region and at a site downstream of the HIS2 gene and that the DSBs are dependent upon genes required for recombination. The frequency of DSBs at HIS2 increases when the gene conversion frequency is increased by alterations in the DNA around HIS2, and vice versa. A deletion that increases both DSBs and conversion can stimulate both when heterozygous; that is, it is semidominant and acts to stimulate DSBs in trans. These data are consistent with the view that homologous chromosomes associate with each other before the formation of the DSBs.The mechanism whereby homologous chromosomes find each other during meiosis and initiate recombination has been the source of considerable speculation and experimentation. Several models have been proposed to account for the genetic and, more recently, molecular data that have been obtained about meiotic recombination. The classical Holliday model (1) suggested that nicks are made in strands of the same polarity in two homologs, after which the broken strands are exchanged from one duplex to the other. The Meselson-Radding model (2) begins recombination with a single strand nick on one homolog, after which one end of the broken strand invades the homologous duplex. More recently, the double strand break (DSB) model for recombination was proposed by Szostak et al. (3); in this scheme, both ends of the broken duplex invade the homolog to initiate recombination. In the latter two models, one can imagine that the mechanism whereby homologs find each other involves recA-like (4) synaptase-assisted searching by the single strands created at the initiating breaks or nicks.Since the publication of the DSB model, experiments have been done that demonstrate that DSBs occur during meiosis in yeast and that they are associated with recombination. These experiments may be sorted into two groups: (i) experiments that examine recombination hot spots both for recombination and DSBs, and (ii) experiments that look at the more global distribution of DSBs along entire chromosomes. Within the first class of experiments, Sun et al. (5) first demonstrated that a meiotic DSB occurs at the ARG4 locus. The location of the DSB was in the DNA sequences that had been shown to be necessary (6) for conversion at ARG4. Furthermore, the time at which the breaks appeared was consistent with the time at which commitment to recombination occurred. In these early experiments, the DSBs were difficult to detect, in part because they were transien...

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“…Of the two proteins encoded on the suppressor plasmid, Rec104p functions in meiosis, where it is necessary for the initiation of meiotic recombination (Galbraith and Malone 1993), whereas Kel1p is a kelch domain-containing protein that functions in both mating and mitosis. Kel1p was identified as a suppressor of the cell fusion defect caused by overactive Pkc1p, but its function in mating remained unclear (Philips and Herskowitz 1998).…”

Section: Isolation Of High-copy Suppressors Of Fus2-l674amentioning

confidence: 99%

Kel1p Mediates Yeast Cell Fusion Through a Fus2p- and Cdc42p-Dependent Mechanism

Smith¹,

Rose

2016

Genetics

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Cell fusion is ubiquitous among eukaryotes. Although little is known about the molecular mechanism, several proteins required for cell fusion in the yeast Saccharomyces cerevisiae have been identified. Fus2p, a key regulator of cell fusion, localizes to the shmoo tip in a highly regulated manner. C-terminal truncations of Fus2p cause mislocalization and fusion defects, which are suppressed by overexpression of Kel1p, a kelch-domain protein of unknown function previously implicated in cell fusion. We hypothesize that Fus2p mislocalization is caused by auto-inhibition, which is alleviated by Kel1p overexpression. Previous work showed that Fus2p localization is mediated by both Fus1p-and actin-dependent pathways. We show that the C-terminal mutations mainly affect the actindependent pathway. Suppression of the Fus2p localization defect by Kel1p is dependent upon Fus1p, showing that suppression does not bypass the normal pathway. Kel1p and a homolog, Kel2p, are required for efficient Fus2p localization, acting through the actindependent pathway. Although Kel1p overexpression can weakly suppress the mating defect of a FUS2 deletion, the magnitude of suppression is allele specific. Therefore, Kel1p augments, but does not bypass, Fus2p function. Fus2p mediates cell fusion by binding activated Cdc42p. Although Kel1p overexpression suppresses a Cdc42p mutant that is defective for Fus2p binding, cell fusion remains dependent upon Fus2p. These data suggest that Fus2p, Cdc42p, and Kel1p form a ternary complex, which is stabilized by Kel1p. Supporting this hypothesis, Kel1p interacts with two domains of Fus2p, partially dependent on Cdc42p. We conclude that Kel1p enhances the activity of Fus2p/Cdc42p in cell fusion.

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Characterization of REC104, a gene required for early meiotic recombination in the yeast Saccharomyces cerevisiae

Cited by 27 publications

References 37 publications

The location and structure of double-strand DNA breaks induced during yeast meiosis: evidence for a covalently linked DNA-protein intermediate.

The location and structure of double-strand DNA breaks induced during yeast meiosis: evidence for a covalently linked DNA-protein intermediate.

Double strand breaks at the HIS2 recombination hot spot in Saccharomyces cerevisiae

Kel1p Mediates Yeast Cell Fusion Through a Fus2p- and Cdc42p-Dependent Mechanism

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