scholarly journals Ndj1, a Telomere-Associated Protein, Promotes Meiotic Recombination in Budding Yeast

2006 ◽  
Vol 26 (10) ◽  
pp. 3683-3694 ◽  
Author(s):  
Hsin-Yen Wu ◽  
Sean M. Burgess
Keyword(s):  
Meiotic Recombination ◽  
Double Strand Breaks ◽  
Homology Search ◽  
Strand Breaks ◽  
Homologous Chromosomes ◽  
Synaptonemal Complex Formation ◽  
Strand Invasion ◽  
Double Holliday Junction ◽  
Meiosis I

ABSTRACT Dynamic telomere repositioning is a prominent feature of meiosis. Deletion of a telomere-associated protein, Ndj1, results in the failure of both attachment and clustering of telomeres at the nuclear envelope and delays several landmarks of meiosis I, such as pairing, synaptonemal complex formation, and timing of the meiosis I division. We explored the role of Ndj1 in meiotic recombination, which occurs through the formation and repair of programmed double-strand breaks. The ndj1Δ mutation allows for the formation of the first detectable strand invasion intermediate (i.e., single-end invasion) with wild-type kinetics; however, it confers a delay in the formation of the double-Holliday junction intermediate and both crossover and noncrossover products. These results challenge the widely held notion that clustering of telomeres in meiosis promotes the ability of homologous chromosomes to find one another in budding Saccharomyces cerevisiae. We propose that an Ndj1-dependent function is critical for stabilizing analogous strand invasion intermediates that exist in two separate branches of the bifurcated pathway, leading to either noncrossover or crossover formation. These findings provide a link between telomere dynamics and a distinct mechanistic step of meiotic recombination that follows the homology search.

scholarly journals The Yeast Motor Protein, Kar3p, Is Essential for Meiosis I

1997 ◽  
Vol 139 (2) ◽  
pp. 459-467 ◽  
Author(s):  
Carol A. Bascom-Slack ◽  
Dean S. Dawson
Keyword(s):  
Synaptonemal Complex ◽  
Meiotic Recombination ◽  
Molecular Motor ◽  
Motor Protein ◽  
Double Strand Breaks ◽  
Wild Type ◽  
Strand Breaks ◽  
Homologous Chromosomes ◽  
Low Levels ◽  
Meiosis I

The recognition and alignment of homologous chromosomes early in meiosis is essential for their subsequent segregation at anaphase I; however, the mechanism by which this occurs is unknown. We demonstrate here that, in the absence of the molecular motor, Kar3p, meiotic cells are blocked with prophase monopolar microtubule arrays and incomplete synaptonemal complex (SC) formation. kar3 mutants exhibit very low levels of heteroallelic recombination. kar3 mutants do produce double-strand breaks that act as initiation sites for meiotic recombination in yeast, but at levels severalfold reduced from wild-type. These data are consistent with a meiotic role for Kar3p in the events that culminate in synapsis of homologues.

scholarly journals Mnd1/Hop2 Facilitates Dmc1-Dependent Interhomolog Crossover Formation in Meiosis of Budding Yeast

2006 ◽  
Vol 26 (8) ◽  
pp. 2913-2923 ◽  
Author(s):  
Jill M. Henry ◽  
Raymond Camahort ◽  
Douglas A. Rice ◽  
Laurence Florens ◽  
Selene K. Swanson ◽  
...  
Keyword(s):  
Meiotic Recombination ◽  
Double Mutant ◽  
Repetitive Sequences ◽  
Double Strand Breaks ◽  
Genomic Integrity ◽  
Dna Interactions ◽  
Strand Breaks ◽  
Homologous Chromosomes ◽  
Meiotic Crossover ◽  
Strand Invasion

ABSTRACT During meiosis, each chromosome must pair with its homolog and undergo meiotic crossover recombination in order to segregate properly at the first meiotic division. Recombination in meiosis in Saccharomyces cerevisiae relies on two Escherichia coli recA homologs, Rad51 and Dmc1, as well as the more recently discovered heterodimer Mnd1/Hop2. Meiotic recombination in S. cerevisiae mnd1 and hop2 single mutants is initiated via double-strand breaks (DSBs) but does not progress beyond this stage; heteroduplex DNA, joint molecules, and crossovers are not detected. Whereas hop2 and mnd1 single mutants are profoundly recombination defective, we show that mnd1 rad51, hop2 rad51, and mnd1 rad17 double mutants are able to carry out crossover recombination. Interestingly, noncrossover recombination is absent, indicating a role for Mnd1/Hop2 in the designation of DSBs for noncrossover recombination. We demonstrate that in the rad51 mnd1 double mutant, recombination is more likely to occur between repetitive sequences on nonhomologous chromosomes. Our results support a model in which Mnd1/Hop2 is required for DNA-DNA interactions that help ensure Dmc1-mediated stable strand invasion between homologous chromosomes, thereby preserving genomic integrity.

scholarly journals MEIOK21: a new component of meiotic recombination bridges required for spermatogenesis

2020 ◽  
Vol 48 (12) ◽  
pp. 6624-6639
Author(s):  
Yongliang Shang ◽  
Tao Huang ◽  
Hongbin Liu ◽  
Yanlei Liu ◽  
Heng Liang ◽  
...  
Keyword(s):  
Meiotic Recombination ◽  
Double Strand Breaks ◽  
Strand Exchange ◽  
Homology Search ◽  
Physical Interaction ◽  
Dna Double Strand Breaks ◽  
Dsb Repair ◽  
Chromosome Localization ◽  
Strand Breaks ◽  
Homologous Chromosomes

Abstract Repair of DNA double-strand breaks (DSBs) with homologous chromosomes is a hallmark of meiosis that is mediated by recombination ‘bridges’ between homolog axes. This process requires cooperation of DMC1 and RAD51 to promote homology search and strand exchange. The mechanism(s) regulating DMC1/RAD51-ssDNA nucleoprotein filament and the components of ‘bridges’ remain to be investigated. Here we show that MEIOK21 is a newly identified component of meiotic recombination bridges and is required for efficient formation of DMC1/RAD51 foci. MEIOK21 dynamically localizes on chromosomes from on-axis foci to ‘hanging foci’, then to ‘bridges’, and finally to ‘fused foci’ between homolog axes. Its chromosome localization depends on DSBs. Knockout of Meiok21 decreases the numbers of HSF2BP and DMC1/RAD51 foci, disrupting DSB repair, synapsis and crossover recombination and finally causing male infertility. Therefore, MEIOK21 is a novel recombination factor and probably mediates DMC1/RAD51 recruitment to ssDNA or their stability on chromosomes through physical interaction with HSF2BP.

scholarly journals End-resection at DNA double-strand breaks in the three domains of life

2013 ◽  
Vol 41 (1) ◽  
pp. 314-320 ◽  
Author(s):  
John K. Blackwood ◽  
Neil J. Rzechorzek ◽  
Sian M. Bray ◽  
Joseph D. Maman ◽  
Luca Pellegrini ◽  
...  
Keyword(s):  
Dna Repair ◽  
Homologous Recombination ◽  
Strand Break ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Homologous Chromosomes ◽  
Domains Of Life ◽  
Strand Invasion ◽  
End Resection

During DNA repair by HR (homologous recombination), the ends of a DNA DSB (double-strand break) must be resected to generate single-stranded tails, which are required for strand invasion and exchange with homologous chromosomes. This 5′–3′ end-resection of the DNA duplex is an essential process, conserved across all three domains of life: the bacteria, eukaryota and archaea. In the present review, we examine the numerous and redundant helicase and nuclease systems that function as the enzymatic analogues for this crucial process in the three major phylogenetic divisions.

scholarly journals Massive crossover elevation via combination of HEI10 and recq4a recq4b during Arabidopsis meiosis

2018 ◽  
Vol 115 (10) ◽  
pp. 2437-2442 ◽  
Author(s):  
Heïdi Serra ◽  
Christophe Lambing ◽  
Catherine H. Griffin ◽  
Stephanie D. Topp ◽  
Divyashree C. Nageswaran ◽  
...  
Keyword(s):  
Meiotic Recombination ◽  
Homologous Chromosome ◽  
Crop Improvement ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Dsb Repair ◽  
Strand Breaks ◽  
Homologous Chromosomes ◽  
Meiotic Dsbs ◽  
Competing Pathways

During meiosis, homologous chromosomes undergo reciprocal crossovers, which generate genetic diversity and underpin classical crop improvement. Meiotic recombination initiates from DNA double-strand breaks (DSBs), which are processed into single-stranded DNA that can invade a homologous chromosome. The resulting joint molecules can ultimately be resolved as crossovers. In Arabidopsis, competing pathways balance the repair of ∼100–200 meiotic DSBs into ∼10 crossovers per meiosis, with the excess DSBs repaired as noncrossovers. To bias DSB repair toward crossovers, we simultaneously increased dosage of the procrossover E3 ligase gene HEI10 and introduced mutations in the anticrossovers helicase genes RECQ4A and RECQ4B. As HEI10 and recq4a recq4b increase interfering and noninterfering crossover pathways, respectively, they combine additively to yield a massive meiotic recombination increase. Interestingly, we also show that increased HEI10 dosage increases crossover coincidence, which indicates an effect on interference. We also show that patterns of interhomolog polymorphism and heterochromatin drive recombination increases distally towards the subtelomeres in both HEI10 and recq4a recq4b backgrounds, while the centromeres remain crossover suppressed. These results provide a genetic framework for engineering meiotic recombination landscapes in plant genomes.

scholarly journals CRISPR targeting of MEIOTIC-TOPOISOMERASE VIB-dCas9 to a recombination hotspot is insufficient to increase crossover frequency in Arabidopsis

2021 ◽  
Author(s):  
Nataliya E. Yelina ◽  
Sabrina Gonzalez-Jorge ◽  
Dominique Hirsz ◽  
Ziyi Yang ◽  
Ian R. Henderson
Keyword(s):  
Meiotic Recombination ◽  
Crop Improvement ◽  
Double Strand Breaks ◽  
Crossover Frequency ◽  
Dna Double Strand Breaks ◽  
Crop Breeding ◽  
Catalytic Subunits ◽  
Strand Breaks ◽  
Homologous Chromosomes ◽  
Meiotic Crossover

AbstractDuring meiosis, homologous chromosomes pair and recombine, which can result in reciprocal crossovers that increase genetic diversity. Crossovers are unevenly distributed along eukaryote chromosomes and show repression in heterochromatin and the centromeres. Within the chromosome arms crossovers are often concentrated in hotspots, which are typically in the kilobase range. The uneven distribution of crossovers along chromosomes, together with their low number per meiosis, creates a limitation during crop breeding, where recombination can be beneficial. Therefore, targeting crossovers to specific genome locations has the potential to accelerate crop improvement. In plants, meiotic crossovers are initiated by DNA double strand breaks (DSBs) that are catalysed by SPO11 complexes, which consist of two catalytic (SPO11-1 and SPO11-2) and two non-catalytic subunits (MTOPVIB). We used the model plant Arabidopsis thaliana to target a dCas9-MTOPVIB fusion protein to the 3a crossover hotspot via CRISPR. We observed that this was insufficient to significantly change meiotic crossover frequency or pattern within 3a. We discuss the implications of our findings for targeting meiotic recombination within plant genomes.

scholarly journals SPO16 binds SHOC1 to promote homologous recombination and crossing-over in meiotic prophase I

2019 ◽  
Vol 5 (1) ◽  
pp. eaau9780 ◽  
Author(s):  
Qianting Zhang ◽  
Shu-Yan Ji ◽  
Kiran Busayavalasa ◽  
Chao Yu
Keyword(s):  
Homologous Recombination ◽  
Meiotic Recombination ◽  
Double Strand Breaks ◽  
Crossing Over ◽  
Dna Double Strand Breaks ◽  
Dsb Repair ◽  
Strand Breaks ◽  
Homologous Chromosomes ◽  
Recombination Nodules ◽  
Evolutionarily Conserved

Segregation of homologous chromosomes in meiosis I is tightly regulated by their physical links, or crossovers (COs), generated from DNA double-strand breaks (DSBs) through meiotic homologous recombination. In budding yeast, three ZMM (Zip1/2/3/4, Mer3, Msh4/5) proteins, Zip2, Zip4, and Spo16, form a “ZZS” complex, functioning to promote meiotic recombination via a DSB repair pathway. Here, we identified the mammalian ortholog of Spo16, termed SPO16, which interacts with the mammalian ortholog of Zip2 (SHOC1/MZIP2), and whose functions are evolutionarily conserved to promote the formation of COs. SPO16 localizes to the recombination nodules, as SHOC1 and TEX11 do. SPO16 is required for stabilization of SHOC1 and proper localization of other ZMM proteins. The DSBs formed in SPO16-deleted meiocytes were repaired without COs formation, although synapsis is less affected. Therefore, formation of SPO16-SHOC1 complex–associated recombination intermediates is a key step facilitating meiotic recombination that produces COs from yeast to mammals.

scholarly journals Mouse TEX15 is essential for DNA double-strand break repair and chromosomal synapsis during male meiosis

2008 ◽  
Vol 180 (4) ◽  
pp. 673-679 ◽  
Author(s):  
Fang Yang ◽  
Sigrid Eckardt ◽  
N. Adrian Leu ◽  
K. John McLaughlin ◽  
Peijing Jeremy Wang
Keyword(s):  
Meiotic Recombination ◽  
Strand Break ◽  
Male Meiosis ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Homologous Chromosomes ◽  
Recombination Proteins ◽  
Meiotic Chromosomes ◽  
Dna Double Strand Break

During meiosis, homologous chromosomes undergo synapsis and recombination. We identify TEX15 as a novel protein that is required for chromosomal synapsis and meiotic recombination. Loss of TEX15 function in mice causes early meiotic arrest in males but not in females. Specifically, TEX15-deficient spermatocytes exhibit a failure in chromosomal synapsis. In mutant spermatocytes, DNA double-strand breaks (DSBs) are formed, but localization of the recombination proteins RAD51 and DMC1 to meiotic chromosomes is severely impaired. Based on these data, we propose that TEX15 regulates the loading of DNA repair proteins onto sites of DSBs and, thus, its absence causes a failure in meiotic recombination.

scholarly journals Massive crossover elevation via combination of HEI10 and recq4a recq4b during Arabidopsis meiosis

2017 ◽  
Author(s):  
Heïdi Serra ◽  
Christophe Lambing ◽  
Catherine H. Griffin ◽  
Stephanie D. Topp ◽  
Mathilde Séguéla-Arnaud ◽  
...  
Keyword(s):  
Meiotic Recombination ◽  
Homologous Chromosome ◽  
Crop Improvement ◽  
Double Strand Breaks ◽  
Dna Double Strand Breaks ◽  
Dsb Repair ◽  
Strand Breaks ◽  
Homologous Chromosomes ◽  
Meiotic Dsbs ◽  
Competing Pathways

AbstractDuring meiosis homologous chromosomes undergo reciprocal crossovers, which generate genetic diversity and underpin classical crop improvement. Meiotic recombination initiates from DNA double strand breaks, which are processed into single-stranded DNA that can invade a homologous chromosome. The resulting joint molecules can ultimately be resolved as crossovers. In Arabidopsis, competing pathways balance the repair of ∼100–200 meiotic DSBs into ∼10 crossovers per meiosis, with the excess DSBs repaired as non-crossovers. In order to bias DSB repair towards crossovers, we simultaneously increased dosage of the pro-crossover E3 ligase gene HEI10 and introduced mutations in the anti-crossover helicase genes RECQ4A and RECQ4B. As HEI10 and recq4a recq4b increase interfering and non-interfering crossover pathways respectively, they combine additively to yield a massive meiotic recombination increase. Interestingly, we also show that increased HEI10 dosage increases crossover coincidence, which indicates an effect of HEI10 on interference. We also show that patterns of interhomolog polymorphism and heterochromatin drive recombination increases towards the sub-telomeres in both HEI10 and recq4a recq4b backgrounds, while the centromeres remain crossover-suppressed. These results provide a genetic framework for engineering meiotic recombination landscapes in plant genomes.

scholarly journals Repeated strand invasion and extensive branch migration are hallmarks of meiotic recombination

2021 ◽  
Author(s):  
Jasvinder S Ahuja ◽  
Catherine S Harvey ◽  
David L Wheeler ◽  
Michael Lichten
Keyword(s):  
Meiotic Recombination ◽  
Holliday Junctions ◽  
Branch Migration ◽  
Dna Double Strand Breaks ◽  
Strand Breaks ◽  
Strand Invasion ◽  
Break Repair ◽  
Strand Annealing ◽  
Double Holliday Junction ◽  
Dual Mechanism

Currently favored models for meiotic recombination posit that both noncrossover and crossover recombination are initiated by DNA double strand breaks but form by different mechanisms, noncrossovers by synthesis dependent strand annealing, and crossovers by formation and resolution of double Holliday junctions centered around the break. This dual mechanism hypothesis predicts different hybrid DNA patterns in noncrossover and crossover recombinants. We show that these predictions are not upheld, by mapping with unprecedented resolution, parental strand contributions to recombinants at a model locus. Instead, break repair in both noncrossovers and crossovers involves synthesis-dependent strand annealing, often with multiple rounds of strand invasion. Crossover-specific double Holliday junction formation occurs via processes that involve branch migration as an integral feature and that can be separated from break repair itself. These findings reveal meiotic recombination to be a highly dynamic process and prompt a new view of the relationship between crossover and noncrossover recombination.

Sign in / Sign up

Export Citation Format

Share Document