Meiotic Recombination Hotspots

Lichten, Michael; Goldman, Alastair S. H.

doi:10.1146/annurev.ge.29.120195.002231

Cited by 337 publications

(193 citation statements)

References 62 publications

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“…below). Attempts to elucidate the determinants of recombination have identified numerous factors of influence, many of which appear to be conserved across eukaryotes (Lichten and Goldman, 1995;Roeder, 1997;Hassold et al, 2000;Keeney, 2001;Petes, 2001;Page and Hawley, 2003). New hypotheses have emerged, for example, that variation in epigenetic features could explain the variation in the rates of recombination between closely related species (Myers et al, , 2008Ptak et al, 2005;Winckler et al, 2005).…”

Section: Determinants and Correlatesmentioning

confidence: 99%

Recombination rate variation in closely related species

2011

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Despite their importance to successful meiosis and various evolutionary processes, meiotic recombination rates sometimes vary within species or between closely related species. For example, humans and chimpanzees share virtually no recombination hotspot locations in the surveyed portion of the genomes. However, conservation of recombination rates between closely related species has also been documented, raising an apparent contradiction. Here, we evaluate how and why conflicting patterns of recombination rate conservation and divergence may be observed, with particular emphasis on features that affect recombination, and the scale and method with which recombination is surveyed. Additionally, we review recent studies identifying features influencing fine-scale and broad-scale recombination patterns and informing how quickly recombination rates evolve, how changes in recombination impact selection and evolution in natural populations, and more broadly, which forces influence genome evolution.

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Section: Determinants and Correlatesmentioning

confidence: 99%

Recombination rate variation in closely related species

2011

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“…The rate of meiotic recombination varies considerably at different positions in the yeast genome (1,2). This variation reflects differences in the frequency of local meiosis-specific doublestrand DNA breaks (DSBs), the recombination-initiating lesion (3,4) catalyzed by Spo11p and associated proteins (5).…”

Section: Introductionmentioning

confidence: 99%

The histone methylase Set2p and the histone deacetylase Rpd3p repress meiotic recombination at the HIS4 meiotic recombination hotspot in Saccharomyces cerevisiae

et al. 2008

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The rate of meiotic recombination in the yeast Saccharomyces cerevisiae varies widely in different regions of the genome with some genes having very high levels of recombination (hotspots). A variety of experiments done in yeast suggest that hotspots are a feature of chromatin structure rather than a feature of primary DNA sequence. We examined the effects of mutating a variety of enzymes that affect chromatin structure on the recombination activity of the well-characterized HIS4 hotspot including the Set2p and Dot1p histone methylases, the Hda1p and Rpd3p histone deacetylases, the Sin4p global transcription regulator, and a deletion of one of the two copies of the genes encoding histone H3-H4. Loss of Set2p or Rpd3p substantially elevated HIS4 hotspot activity, and loss of Hda1p had a smaller stimulatory effect; none of the other alterations had a significant effect. The increase of HIS4 hotspot activity in set2 and rpd3 strains is likely to be related to the recent finding that histone H3 methylation by Set2p directs deacetylation of histones by Rpd3p. IntroductionThe rate of meiotic recombination varies considerably at different positions in the yeast genome (1,2). This variation reflects differences in the frequency of local meiosis-specific doublestrand DNA breaks (DSBs), the recombination-initiating lesion (3,4) catalyzed by Spo11p and associated proteins (5). There are several lines of evidence that the frequency of DSBs is regulated by elements of chromatin structure rather than primary DNA sequence (2). First, recombination hotspots exhibit hypersensitivity to nucleases (6-10). Some loci (8,9) undergo meiosis-specific alterations in nuclease sensitivity prior to DSB formation, although no such changes are observed at other loci (6). Since all nuclease-hypersensitive regions are not meiotic Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Conflicts of interest None. NIH Public AccessAuthor Manuscript DNA Repair (Amst) (6,10), "open" chromatin appears necessary, but not sufficient, for meiotic recombination hotspot activity. Second, insertion of a nucleosome-excluding sequence into the yeast genome creates a recombination hotspot (11). Third, the activity of some hotspots requires the binding of transcription factors, but not high levels of transcription (2). This result has been interpreted as indicating that chromatin modifications associated with transcription factor binding stimulate both transcription and recombination. Finally, some mutants that affect chromatin modifications reduce the frequency of meiosis-specific DSBs. In the yeast S. pombe, mutatio...

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“…Most or all of these recombination events involve a DNA double strand break (DSB) intermediate (Lichten & Goldman 1995). Such intermediates can be detected at certain recombination hot spots by Southern hybridization techniques (Sun et al 1989;Cao et al 1990).…”

Section: Introductionmentioning

confidence: 99%

High copy number suppression of the meiotic arrest caused by a dmc1 mutation: REC114 imposes an early recombination block and RAD54 promotes a DMC1‐independent DSB repair pathway

et al. 1999

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Background: DMC1, the meiosis-speci®c eukaryotic homologue of bacterial recA, is required for completion of meiotic recombination and cell cycle progression past prophase. In a dmc1 mutant, double strand break recombination intermediates accumulate and cells arrest in prophase. We isolated genes which, when present at high copy numbers, suppress the meiotic arrest phenotype conferred by dmc1 mutations.

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Meiotic Recombination Hotspots

Cited by 337 publications

References 62 publications

Recombination rate variation in closely related species

Recombination rate variation in closely related species

The histone methylase Set2p and the histone deacetylase Rpd3p repress meiotic recombination at the HIS4 meiotic recombination hotspot in Saccharomyces cerevisiae

High copy number suppression of the meiotic arrest caused by a dmc1 mutation: REC114 imposes an early recombination block and RAD54 promotes a DMC1‐independent DSB repair pathway

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