The Meiotic Recombination Hotspots of Schizosaccharomyces pombe

Pryce, David W.; McFarlane, Ramsay J.

doi:10.1159/000166614

Cited by 5 publications

(7 citation statements)

References 44 publications

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“…Meiotic crossovers tend to form at specific sites in the genome of most organisms (Buard and de Massy, 2007;Mezard, 2006;Pryce and McFarlane, 2009); these are known as recombination hotspots. In mammals, hotspots are typically regions of 1-2 kb that occur every 50-100 kb within the genome (Jeffreys et al, 2001;McVean, 2010;Myers et al, 2008).…”

Section: Control Of Meiotic Dsb Formationmentioning

confidence: 99%

The choice in meiosis – defining the factors that influence crossover or non-crossover formation

Youds

Boulton

2011

Journal of Cell Science

152

132

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Commentary 501 IntroductionMeiosis is the specialised reductive division that generates haploid cells. During this process, a single round of replication is followed by two rounds of chromosome segregation: in the first division (meiosis I), homologous chromosomes segregate, whereas in the second division, sister chromatids segregate (meiosis II). A key step in meiosis I is the recognition of homologous chromosomes, which then align and pair along the length of the chromosome. Once homologues have aligned, synapsis can proceed with the formation of the synaptonemal complex (SC), a protein structure that supports and maintains homologues in close juxtaposition and serves as a scaffold for crossover-promoting recombination factors. Meiotic crossing over involves the generation of meiotic doublestrand breaks (DSBs), which are subsequently repaired either as crossovers or non-crossovers (Fig. 1). Meiotic recombination is not only necessary to create new allele combinations that generate genetic diversity, but is also essential in ensuring accurate chromosome segregation at the first meiotic division because the crossover acts as a tether between homologues, which ensures that each homologue will properly align at the metaphase plate and thereby correctly attach to the spindle. DSB repair occurs concurrently with SC formation and is required for normal synapsis in yeast and mice (Baudat et al., 2000;Roeder, 1997;Romanienko and Camerini-Otero, 2000), whereas in Caenorhabditis elegans and Drosophila melanogaster, homologue pairing and SC formation can occur independently of meiotic recombination (Colaiacovo et al., 2003; Dernburg et al., 1998;Liu et al., 2002;McKim et al., 1998).The process of meiotic recombination is initiated when meiotic DSBs are created by the endonuclease SPO11, in conjunction with a number of additional proteins (Keeney and Neale, 2006). DSBs are then resected to generate 3Ј single-strand DNA (ssDNA) overhangs that are initially bound by replication protein A (RPA), which is subsequently displaced by the recombinase radiation sensitive 51 (RAD51) and/or the meiosis-specific recombinase dosage suppressor of Mck1 (DMC1) to form nucleoprotein filaments. These filaments serve to find a complimentary sequence within a homologous chromosome, at which they instigate singleend strand invasions (Hunter and Kleckner, 2001) to generate socalled displacement loop (D loop) recombination intermediates ( Fig. 1). If the second end of the original DSB binds with the homologous chromosome, a double Holliday junction is formed, which can be resolved to generate either a non-crossover or an interhomologue crossover, the latter of which is hereafter referred to simply as crossover (Bishop and Zickler, 2004;Schwacha and Kleckner, 1995). Double Holliday junctions can also be processed through dissolution, which results in a non-crossover ( Fig. 1) (Wu and Hickson, 2003). Meiotic non-crossovers have also been proposed to form when strand invasion is transient, and when a limited amount of DNA synthesis occurs befor...

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Section: Control Of Meiotic Dsb Formationmentioning

confidence: 99%

The choice in meiosis – defining the factors that influence crossover or non-crossover formation

Youds

Boulton

2011

Journal of Cell Science

152

132

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“…126). Further studies have identified several additional trans -acting factors that are required for activation, including several ATP-dependent chromatin-remodelling factors (including Gcn5, Snf22, Ada2 and Mst2, which activate, and Hrp1 and Hrp3, which act antagonistically) and the transcriptional repressors Tup11 and Tup12, which suppress recombination 127,128 . Further analysis has revealed that the CRE element ATGACGT is appreciably more effective when it resides in an 18-bp consensus element, GNVTATGACGTCATNBNC 63 .…”

Section: Figurementioning

confidence: 99%

Mammalian recombination hot spots: properties, control and evolution

2010

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Recombination, together with mutation, generates the raw material of evolution, is essential for reproduction and lies at the heart of all genetic analysis. Recent advances in our ability to construct genome-scale, high-resolution recombination maps and new molecular techniques for analysing recombination products have substantially furthered our understanding of this important biological phenomenon in humans and mice: from describing the properties of recombination hot spots in male and female meiosis to the recombination landscape along chromosomes. This progress has been accompanied by the identification of trans-acting systems that regulate the location and relative activity of individual hot spots.

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“…[6] for recent review). The ade6-M26 allele promotes specifically meiotic (but not mitotic) recombination [7].…”

Section: Introductionmentioning

confidence: 99%

Phosphorylation-Independent Regulation of Atf1-Promoted Meiotic Recombination by Stress-Activated, p38 Kinase Spc1 of Fission Yeast

2009

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BackgroundStress-activated protein kinases regulate multiple cellular responses to a wide variety of intracellular and extracellular conditions. The conserved, multifunctional, ATF/CREB protein Atf1 (Mts1, Gad7) of fission yeast binds to CRE-like (M26) DNA sites. Atf1 is phosphorylated by the conserved, p38-family kinase Spc1 (Sty1, Phh1) and is required for many Spc1-dependent stress responses, efficient sexual differentiation, and activation of Rec12 (Spo11)-dependent meiotic recombination hotspots like ade6-M26.Methodology/Principal FindingsWe sought to define mechanisms by which Spc1 regulates Atf1 function at the ade6-M26 hotspot. The Spc1 kinase was essential for hotspot activity, but dispensable for basal recombination. Unexpectedly, a protein lacking all eleven MAPK phospho-acceptor sites and detectable phosphorylation (Atf1-11M) was fully proficient for hotspot recombination. Furthermore, tethering of Atf1 to ade6 in the chromosome by a heterologous DNA binding domain bypassed the requirement for Spc1 in promoting recombination.Conclusions/SignificanceThe Spc1 protein kinase regulates the pathway of Atf1-promoted recombination at or before the point where Atf1 binds to chromosomes, and this pathway regulation is independent of the phosphorylation status of Atf1. Since basal recombination is Spc1-independent, the principal function of the Spc1 kinase in meiotic recombination is to correctly position Atf1-promoted recombination at hotspots along chromosomes. We also propose new hypotheses on regulatory mechanisms for shared (e.g., DNA binding) and distinct (e.g., osmoregulatory vs. recombinogenic) activities of multifunctional, stress-activated protein Atf1.

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The Meiotic Recombination Hotspots of Schizosaccharomyces pombe

Cited by 5 publications

References 44 publications

The choice in meiosis – defining the factors that influence crossover or non-crossover formation

The choice in meiosis – defining the factors that influence crossover or non-crossover formation

Mammalian recombination hot spots: properties, control and evolution

Phosphorylation-Independent Regulation of Atf1-Promoted Meiotic Recombination by Stress-Activated, p38 Kinase Spc1 of Fission Yeast

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