Ontology highlight
ABSTRACT:
PROVIDER: PRJNA391770 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5753980_1.fastq.gz | Fastqsanger.gz | |||
| SRR5753980_2.fastq.gz | Fastqsanger.gz | |||
| SRR5753990_1.fastq.gz | Fastqsanger.gz | |||
| SRR5753990_2.fastq.gz | Fastqsanger.gz | |||
| SRR5754000_1.fastq.gz | Fastqsanger.gz |
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Project description:Several protein ensembles facilitate meiotic crossover recombination and the associated process of synaptonemal complex (SC) assembly during meiosis. We have employed proximity labeling as a phenotyping tool to investigate functional requirements for spatial relationships between meiotic recombination and SC proteins in S. cerevisiae, and to gain deeper insight into the molecular deficits of crossover-deficient meiotic mutants. We find that recombination initiation and synaptonemal complex structures are dispensable for proximity labeling of the Zip3 E3 ligase by components of the ZZS ensemble (Zip2, Zip4 and Spo16) but enzymes associated with early steps in recombination are required for Zip3 proximity labeling by MutSg, consistent with the possibility that MutSg joins Zip3 only after a specific recombination intermediate has been generated. Proximity labeling furthermore suggests that a key defect of crossover-defective, SC-proficient zip1 separation-of-function mutants is a failure to assemble an early recombination ensemble where MutSg can properly engage Zip3. We also find that the SC structural protein Ecm11 is proximity labeled by ZZS proteins in a Zip4-dependent and Zip1-independent manner, but by Zip3 and Msh4 at least in part via a distinct pathway that relies on Zip1. Finally, streptavidin pulldown followed by mass spectrometry on eleven proximity labeling strains uncovered shared proximity targets of SC and crossover-associated proteins, some of which have not yet been implicated in meiotic recombination or SC formation highlighting the potential of proximity labeling as a discovery tool.
2024-10-02 | PXD053621 | Pride
Project description:Meiotic recombination promotes genetic diversification as well as pairing and segregation of homologous chromosomes, but the double-strand breaks (DSBs) that initiate recombination are dangerous lesions that can cause mutation or meiotic failure. How cells control DSBs to balance between beneficial and deleterious outcomes is not well understood. This study tests the hypothesis that DSB control involves a network of intersecting regulatory circuits. We show that DSBs form in greater numbers in Saccharomyces cerevisiae cells lacking ZMM proteins, a suite of recombination-promoting factors traditionally regarded as acting strictly downstream of DSB formation. This counterintuitive result suggests that homologous chromosomes that have successfully engaged one another stop making DSBs, and provides new insight into phenotypes of zmm and other recombination-defective mutants. A genetically distinct pathway ties DSB formation to meiotic progression through the Ndt80 transcription factor. High-resolution genome-wide DSB maps generated by sequencing short oligonucleotides covalently bound to Spo11 (Spo11 oligos) demonstrate that feedback tied to ZMM function contributes in unexpected ways to spatial patterning of the recombination landscape. Four samples total: two wild type and two zip3 mutant (each an independent culture)
2014-04-23 | E-GEOD-48299 | biostudies-arrayexpress
Project description:Meiotic recombination promotes genetic diversification as well as pairing and segregation of homologous chromosomes, but the double-strand breaks (DSBs) that initiate recombination are dangerous lesions that can cause mutation or meiotic failure. How cells control DSBs to balance between beneficial and deleterious outcomes is not well understood. This study tests the hypothesis that DSB control involves a network of intersecting regulatory circuits. We show that DSBs form in greater numbers in Saccharomyces cerevisiae cells lacking ZMM proteins, a suite of recombination-promoting factors traditionally regarded as acting strictly downstream of DSB formation. This counterintuitive result suggests that homologous chromosomes that have successfully engaged one another stop making DSBs, and provides new insight into phenotypes of zmm and other recombination-defective mutants. A genetically distinct pathway ties DSB formation to meiotic progression through the Ndt80 transcription factor. High-resolution genome-wide DSB maps generated by sequencing short oligonucleotides covalently bound to Spo11 (Spo11 oligos) demonstrate that feedback tied to ZMM function contributes in unexpected ways to spatial patterning of the recombination landscape.
2014-04-23 | GSE48299 | GEO
Project description:Histone H3K4 methylation is a feature of meiotic recombination hotspots shared by many organisms including plants and mammals. Meiotic recombination is initiated by programmed double-strand break (DSB) formation that in budding yeast takes place in gene promoters and is promoted by histone H3K4 di/trimethylation. This histone modification is recognized by Spp1, a PHD-finger containing protein that belongs to the conserved histone H3K4 methyltransferase Set1 complex. During meiosis, Spp1 binds H3K4me3 and interacts with a DSB protein, Mer2, to promote DSB formation close to gene promoters. How Set1 complex- and Mer2- related functions of Spp1 are connected is not clear. Here, combining genome-wide localization analyses, biochemical approaches and the use of separation of function mutants, we show that Spp1 is present within two distinct complexes in meiotic cells, the Set1 and the Mer2 complexes. Disrupting the Spp1-Set1 interaction mildly decreases H3K4me3 levels and does not affect meiotic recombination initiation. Conversely, the Spp1-Mer2 interaction is required for normal meiotic recombination initiation, but dispensable for Set1 complex-mediated histone H3K4 methylation. Finally, we provide evidence that Spp1 preserves normal H3K4me3 levels independently of the Set1 complex. We propose a model where Spp1 works in three ways to promote recombination initiation: first by depositing histone H3K4 methylation (Set1 complex), next by “reading” and protecting histone H3K4 methylation, and finally by making the link with the chromosome axis (Mer2-Spp1 complex). This work deciphers the precise roles of Spp1 in meiotic recombination and opens perspectives to study its functions in other organisms where H3K4me3 is also present at recombination hotspots.
2017-11-30 | GSE102790 | GEO
Project description:DNA double-strand breaks (DSBs) initiate meiotic recombination. Past DSB-mapping studies have used rad50S or sae2? mutants, which are defective in break processing, to accumulate DSBs, and report large (= 50 kb) “DSB-hot” regions that are separated by “DSB-cold” domains of similar size. Substantial recombination occurs in some DSB-cold regions, suggesting that DSB patterns are not normal in rad50S or sae2? mutants. We therefore developed novel methods that detect DSBs using ssDNA enrichment and microarray hybridization, and that use background-based normalization to allow cross-comparison between array datasets, to map genome-wide the DSBs that accumulate in processing-capable, repair-defective dmc1î and dmc1î rad51î mutants. DSBs were observed at known hotspots, but also in most previously-identified “DSB-cold” regions, including near centromeres and telomeres. While about 40% of the genome is DSB-cold in rad50S mutants, analysis of meiotic ssDNA from dmc1? shows that most of these regions have significant DSB activity. Thus, DSBs are distributed much more uniformly than was previously believed. Southern-blot assays of DSBs in selected regions in dmc1?, rad50S and wild-type cells confirm these findings. Comparisons of DSB signals in dmc1, dmc1 rad51, and dmc1 spo11 mutant strains identify Dmc1 as the primary strand transfer activity genome-wide, and Spo11-induced lesions as initiating all meiotic recombination. Keywords: DSB mapping, ChIP-chip, single strand DNA , BND cellulose
2007-12-31 | GSE8981 | GEO
Project description:DNA double-strand breaks (DSBs) initiate meiotic recombination. Past DSB-mapping studies have used rad50S or sae2? mutants, which are defective in break processing, to accumulate DSBs, and report large (= 50 kb) “DSB-hot” regions that are separated by “DSB-cold” domains of similar size. Substantial recombination occurs in some DSB-cold regions, suggesting that DSB patterns are not normal in rad50S or sae2? mutants. We therefore developed novel methods that detect DSBs using ssDNA enrichment and microarray hybridization, and that use background-based normalization to allow cross-comparison between array datasets, to map genome-wide the DSBs that accumulate in processing-capable, repair-defective dmc1î and dmc1î rad51î mutants. DSBs were observed at known hotspots, but also in most previously-identified “DSB-cold” regions, including near centromeres and telomeres. While about 40% of the genome is DSB-cold in rad50S mutants, analysis of meiotic ssDNA from dmc1? shows that most of these regions have significant DSB activity. Thus, DSBs are distributed much more uniformly than was previously believed. Southern-blot assays of DSBs in selected regions in dmc1?, rad50S and wild-type cells confirm these findings. Comparisons of DSB signals in dmc1, dmc1 rad51, and dmc1 spo11 mutant strains identify Dmc1 as the primary strand transfer activity genome-wide, and Spo11-induced lesions as initiating all meiotic recombination. Keywords: DSB mapping, ChIP-chip, single strand DNA , BND cellulose We use two different strategies to map the genome-wide distribution of meiotic DSBs in the yeast Saccharomyces cerevisiae. The first is a chromatin immunoprecipitation (ChIP) based approach that targets the Spo11p protein, which remains covalently attached to DSB ends in the rad50S mutant background. The second approach involves BND cellulose enrichment of the single strand DNA (ssDNA) recombination intermediate formed by end-resection at DSB sites following Spo11p removal. We use dmc1 and dmc1 rad51 mutants that accumulates meiotic single strand DNA intermediates
2007-12-30 | E-GEOD-8981 | biostudies-arrayexpress
Project description:During meiosis, Structural Maintenance of Chromosome (SMC) complexes underpin two fundamental features of meiosis: homologous recombination and chromosome segregation. While meiotic functions of the cohesin and condensin complexes have been delineated, the role of the third SMC complex, Smc5/6, remains enigmatic. Diminished Smc5/6 function causes severe defects in nuclear division, but the underlying causes of these defects remain unclear. Here we identify specific, essential meiotic functions for the Smc5/6 complex in homologous recombination and regulation of cohesin. We show that Smc5/6 is enriched at centromeres and cohesin-association sites where it regulates sister-chromatid cohesion and the timely removal of cohesin from chromosomal arms, respectively. Smc5/6 also localizes to recombination hotspots, where it promotes normal formation and resolution of joint-molecule intermediates. Furthermore, we find that Smc5/6 specifically promotes resolution of joint molecules via the XPF-family endonuclease, Mus81-Mms4Eme1. We propose that Smc5/6 acts as a chaperone for ‘mitotic’-like recombination processes during meiosis.
2013-12-27 | GSE44852 | GEO
Project description:Meiotic recombination is initiated by the Spo11 endonuclease, which directs DNA double strand breaks at discrete regions in the genome coined hotspots. Here we report the profiles and dynamics of histone modifications at the cores of mouse recombination hotspots in early meiotic prophase. To define the spectrum of possible regulators of histone methylation and acetylation at all stages of meiosis I, expression analyses of histone acetylases/deacetylases (HATs/HDACs) and and HMTs/HDMTs genes when comparing those expressed in spermatogonia, pre-leptotene and leptotene/zygotene versus pachytene meiotic stages.
2016-11-04 | GSE57197 | GEO