Saccharomyces cerevisiae S288c X YJM789
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA246635 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR1297120_1.fastq.gz | Fastqsanger.gz | |||
| SRR1297120_2.fastq.gz | Fastqsanger.gz | |||
| SRR1297130_1.fastq.gz | Fastqsanger.gz | |||
| SRR1297130_2.fastq.gz | Fastqsanger.gz | |||
| SRR1297140_1.fastq.gz | Fastqsanger.gz |
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Project description:Meiotic recombination promotes genomic diversity by generating new combinations of alleles, while at the same time, maintaining genome stability by preventing chromosome missegregation and aneuploidy, such as Down Syndrome. We report here the first genome-wide maps of meiotic recombination in the human female meiosis. By utilizing information from all three meiotic products (oocyte, polar body 1 and polar body 2), our data reveal crossover rates that are in great excess (~40%) of recombination rate estimates from population-based studies. Recovery of all three meiotic products allowed us to identify structural defects to meiotic chromosomes that originate during meiosis, as well as true meiotic drive at meiosis II for the preferential exclusion of non-recombinant chromatids from the oocyte. Finally, we identify a novel chromosome segregation pattern reminiscent of 'inverted meiosis' that leads to chromosomally-balanced oocytes. The three products of meiosis from 13 oocytes and the gDNA from the five donors were analysed (total of 44 samples). Blank (negative) and positive (genomic DNA) control samples were provided for each DNA amplifiction run. No replicates were included as they were not available. No external references were included.
2015-03-01 | E-GEOD-53539 | biostudies-arrayexpress
Project description:Interference exists ubiquitously in many biological processes. Crossover interference patterns meiotic crossovers, which are required for faithful chromosome segregation and evolutionary adaption. However, what the interference signal is and how it is generated and regulated are unknown. We show that yeast top2 alleles cannot bind or cleave DNA accumulate a higher level of negative supercoils and show weaker interference. However, top2 alleles cannot religate the cleaved DNA or release the religated DNA accumulate less negative supercoils and show stronger interference. Moreover, the level of negative supercoils is negatively correlated with crossover interference strength in various strains. Furthermore, negative supercoils preferentially enrich at crossover-associated Zip3 regions before the formation of meiotic DNA double-strand breaks, and regions with more negative supercoils tend to have more Zip3. Additionally, the strength of crossover interference and homeostasis change coordinately in mutants. These findings suggest that the accumulation and relief of negative supercoils pattern meiotic crossovers.
2022-08-24 | GSE201366 | GEO
Project description:During meiosis, crossover recombination is essential to link homologous chromosomes and drive faithful chromosome segregation. Crossover recombination is non-random across the genome, and centromere-proximal crossovers are associated with an increased risk of aneuploidy, including Trisomy 21 in humans. Here, we identify the conserved Ctf19/CCAN kinetochore sub-complex as a major factor that minimizes potentially deleterious centromere-proximal crossovers in budding yeast. We uncover multi-layered suppression of pericentromeric recombination by the Ctf19 complex, operating across distinct chromosomal distances. The Ctf19 complex prevents meiotic DNA break formation, the initiating event of recombination, proximal to the centromere. The Ctf19 complex independently drives the enrichment of cohesin throughout the broader pericentromere to suppress crossovers, but not DNA breaks. This non-canonical role of the kinetochore in defining a chromosome domain that is refractory to crossovers adds a new layer of functionality by which the kinetochore prevents the incidence of chromosome segregation errors that generate aneuploid gametes.
2015-12-15 | GSE72683 | GEO
Project description:Faithful meiotic chromosome inheritance and fertility relies on the stimulation of meiotic crossover recombination by potentially genotoxic DNA double-strand breaks (DSBs). To avoid excessive damage, feedback mechanisms down-regulate DSBs on chromosomes that have successfully initiated crossover repair. In Saccharomyces cerevisiae, this regulation requires the removal of the conserved DSB-promoting protein Hop1/HORMAD during chromosome synapsis. Here, we identify privileged end-adjacent regions (EARs) spanning roughly 100 Kb near all telomeres that escape DSB downregulation. These regions retain Hop1 and continue to break in pachynema despite normal synaptonemal complex deposition. Differential retention of Hop1 requires the disassemblase Pch2/TRIP13, which preferentially removes Hop1 from telomere-distant sequences, and is modulated by the histone deacetylase Sir2 and the nucleoporin Nup2. Importantly, the uniform size of EARs among chromosomes contributes to disproportionately high DSB and repair signals on short chromosomes in pachynema, suggesting that EARs partially underlie the curiously high recombination rate of short chromosomes. Grant ID: Research grant #6-FY16-208 Grant title: Meiotic segregation of small chromosomes Funding Source: March of Dimes Foundation Affiliation: NEW YORK UNIVERSITY Name: Andreas Hochwagen
2019-01-10 | GSE105111 | GEO
Project description:During meiosis, crossover recombination is essential to link homologous chromosomes and drive faithful chromosome segregation. Crossover recombination is non-random across the genome, and centromere-proximal crossovers are associated with an increased risk of aneuploidy, including Trisomy 21 in humans. Here, we identify the conserved Ctf19/CCAN kinetochore sub-complex as a major factor that minimizes potentially deleterious centromere-proximal crossovers in budding yeast. We uncover multi-layered suppression of pericentromeric recombination by the Ctf19 complex, operating across distinct chromosomal distances. The Ctf19 complex prevents meiotic DNA break formation, the initiating event of recombination, proximal to the centromere. The Ctf19 complex independently drives the enrichment of cohesin throughout the broader pericentromere to suppress crossovers, but not DNA breaks. This non-canonical role of the kinetochore in defining a chromosome domain that is refractory to crossovers adds a new layer of functionality by which the kinetochore prevents the incidence of chromosome segregation errors that generate aneuploid gametes. Two samples total: two biological replicate Spo11-oligo maps of S. cerevisiae SK1 mcm21 null mutant
2015-12-15 | E-GEOD-72683 | biostudies-arrayexpress
Project description:The data set submitted here contains the raw SNP genotyping data obtained from the analysis of 24 biparental segregating maize (Zea mays L.) populations and their respective parents. The processed and filtered data were used to construct genetic linkage maps which we used in our study of variation of recombination rate in maize. In sexually reproducing organisms, meiotic crossovers ensure the proper segregation of chromosomes and contribute to genetic diversity by shuffling allelic combinations. Such genetic reassortment is exploited in breeding to combine favorable alleles, and in genetic research to identify genetic factors underlying traits of interest via linkage or association-based approaches. Crossover numbers and distributions along chromosomes vary between species, but little is known about their intraspecies variation. In our study, we report on the variation of recombination rates between 22 European maize inbred lines that belong to the Dent and Flint gene pools. We genotyped 23 doubled-haploid populations derived from crosses between these lines with a 50k-SNP array and constructed high-density genetic maps, showing good correspondence with the maize B73 genome sequence assembly. By aligning each genetic map to the B73 sequence, we obtained the recombination rates along chromosomes specific to each population. We identified significant differences in recombination rates at the genome-wide, chromosome, and intrachromosomal levels between populations, as well as significant variation for genome-wide recombination rates among maize lines. Crossover interference analysis using a two-pathway modeling framework revealed a negative association between recombination rate and interference strength. To our knowledge, the present work provides the most comprehensive study on intraspecific variation of recombination rates and crossover interference strength in eukaryotes. Differences found in recombination rates will allow for selection of high or low recombining lines in crossing programs. Our methodology should pave the way for precise identification of genes controlling recombination rates in maize and other organisms.
2013-09-05 | GSE50558 | GEO
Project description:During gamete formation, crossover recombination must occur on replicated DNA to ensure proper chromosome segregation in the first meiotic division. We identified a Mec1/ATR-dependent replication checkpoint in budding yeast that prevented the earliest stage of recombination, the programmed induction of DNA double-strand breaks (DSBs), when pre-meiotic DNA replication was delayed. The checkpoint suppressed DSBs through three complementary mechanisms: inhibition of Mer2 phosphorylation by Dbf4-dependent Cdc7 kinase, preclusion of chromosomal loading of Rec114 and Mre11, and lowered abundance of the Spo11 nuclease. Without this checkpoint, cells formed DSBs on partially replicated chromosomes. Importantly, such DSBs frequently failed to be repaired and impeded further DNA synthesis, leading to a rapid loss in cell viability. We conclude that a checkpoint-dependent constraint of DSB formation to duplicated DNA is critical not only for meiotic chromosome assortment, but also to protect genome integrity during gametogenesis.
2013-09-20 | GSE46841 | GEO
Project description:Meiotic crossover formation requires the stabilization of early recombination intermediates by a set of proteins and occurs within the environment of the chromosome axis, a structure important for the regulation of meiotic recombination events. The molecular mechanisms underlying and connecting crossover recombination and axis localization are elusive. Here, we identified the ZZS (Zip2–Zip4–Spo16) complex, required for crossover formation, which carries two distinct activities: one provided by Zip4, which acts as hub through physical interactions with components of the chromosome axis and the crossover machinery, and the other carried by Zip2 and Spo16, which preferentially bind branched DNA molecules in vitro. We found that Zip2 and Spo16 share structural similarities to the structure-specific XPF–ERCC1 nuclease, although it lacks endonuclease activity. The XPF domain of Zip2 is required for crossover formation, suggesting that, together with Spo16, it has a noncatalytic DNA recognition function. Our results suggest that the ZZS complex shepherds recombination intermediates toward crossovers as a dynamic structural module that connects recombination events to the chromosome axis. The identification of the ZZS complex improves our understanding of the various activities required for crossover implementation and is likely applicable to other organisms, including mammals.
2018-02-14 | GSE103877 | GEO
Project description:Meiotic crossover (CO) serves dual essential roles in ensuring accurate chromosome segregation and generating genetic diversity. While protein ubiquitination has been implicated in meiotic CO formation, the specific E3 ligases involved and their molecular mechanisms remain largely characterized. Through systematic screening, we identified Ufd2p as a key meiotic CO regulator. Depletion of Ufd2p severely impaired meiotic recombination by reducing CO numbers and enhancing CO interference strength. Multi-omics analysis identified topoisomerase II (Top2p) as a specific substrate of Ufd2p, and Ufd2p could catalyze Top2p ubiquitination to promote its degradation through ubiquitin-proteasome pathway. Accumulated Top2p in Ufd2p depletion strains resolves DNA negative supercoils, which in turn enhances CO interference strength and reduces CO numbers. Remarkably, expression of either mouse or human UBE4B in yeast effectively rescued the meiotic and recombination defects caused by Ufd2p depletion. These findings provide important insights into the ubiquitin-mediated regulatory network governing chromatin structure and meiotic recombination pattern
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Project description:During gamete formation, crossover recombination must occur on replicated DNA to ensure proper chromosome segregation in the first meiotic division. We identified a Mec1/ATR-dependent replication checkpoint in budding yeast that prevented the earliest stage of recombination, the programmed induction of DNA double-strand breaks (DSBs), when pre-meiotic DNA replication was delayed. The checkpoint suppressed DSBs through three complementary mechanisms: inhibition of Mer2 phosphorylation by Dbf4-dependent Cdc7 kinase, preclusion of chromosomal loading of Rec114 and Mre11, and lowered abundance of the Spo11 nuclease. Without this checkpoint, cells formed DSBs on partially replicated chromosomes. Importantly, such DSBs frequently failed to be repaired and impeded further DNA synthesis, leading to a rapid loss in cell viability. We conclude that a checkpoint-dependent constraint of DSB formation to duplicated DNA is critical not only for meiotic chromosome assortment, but also to protect genome integrity during gametogenesis. DSB factor association was measured in wild-type and checkpoint mutants strains under non-inducing or replication checkpoint inducing conditions. Additionally, DNA replication and helicase loading were measured in a replication and checkpoint deficient strain (cdc6-mn).
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