Essential roles of the ANKRD31-REC114 interaction in meiotic recombination and mouse spermatogenesis
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ABSTRACT:
PROVIDER: PRJNA954468 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR24136612_1.fastq.gz | Fastqsanger.gz | |||
| SRR24136612_2.fastq.gz | Fastqsanger.gz | |||
| SRR24136613_1.fastq.gz | Fastqsanger.gz | |||
| SRR24136613_2.fastq.gz | Fastqsanger.gz | |||
| SRR24136614_1.fastq.gz | Fastqsanger.gz |
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Project description:DNA double-strand breaks (DSBs) initiate meiotic recombination. ANKRD31 recently emerged as a DSB regulator particularly important in the pseudoautosomal regions (PARs) of sex chromosomes. ANKRD31 interacts with multiple proteins, including DSB-promoting REC114. To test if this interaction is important, we generated mice with Ankrd31 mutations that either reduced (missense) or eliminated (C-terminal truncation) the ANKRD31–REC114 interaction without diminishing contacts with other partners. Eliminating the interaction mimicked an Ankrd31 null, with delayed DSB formation, defective DSB repair, and altered DSB locations including absence of PAR breaks. When the ANKRD31–REC114 interaction was instead attenuated, DSB formation was again delayed globally, but DSB locations and repair were affected little if at all. The missense Ankrd31 allele showed a dosage effect, wherein combining it with the null or C-terminal truncation allele resulted in intermediate phenotypes. Our results show that ANKRD31 function is critically dependent on its interaction with REC114, and that defects in ANKRD31 activity correlate with the severity of interaction disruption.
2023-04-18 | GSE229450 | GEO
Project description:Meiotic recombination is initiated by the Spo11 endonuclease, which directs DNA DSBs. We report here that the recombinogenic cores of active hotspots in mice harbor several histone H3 and H4 acetylation and methylation marks that are typical of open, active chromatin. Further, deposition of these histone marks is dynamic and manifest at spermatogonia and/or pre-leptotene meiotic cells, which would facilitate the formation of DSBs at leptotene. Importantly, there was concordance in the overlap of the histone mark ChIP profiles with nucleosome occupancy maps, which were determined by real-time PCR and whole genome sequencing (WGS) analyses of micococcal-nuclease resistance regions across four mouse meiotic hotspots (HS22, HS59.4, HS59.5 and HS61.1). Our study reveals that there are instructive roles of histone acetylated marks at meiotic recombination hotspot cores and that they are necessary to promote hotspot activity and crossover resolution.
2016-11-04 | GSE87057 | GEO
Project description:Functional Roles of Acetylated Histone Marks at Mouse Meiotic Recombination Hotspots
| PRJNA343465 | ENA
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
Project description:Meiotic recombination between homologous chromosomes initiates via programmed DNA double-strand breaks (DSBs), generated by complexes comprising Spo11 transesterase plus accessory proteins. DSBs arise concomitantly with the development of axial chromosome structures, where the coalescence of axis sites produces linear arrays of chromatin loops. Recombining DNA sequences map to loops, but are ultimately tethered to the underlying axis. How and when such tethering occurs is currently unclear. Using ChIPchip in yeast, we show that Spo11-accessory proteins Rec114, Mer2 and Mei4 stably interact with chromosome axis sequences, upon phosphorylation of Mer2 by S-phase Cdk. This axis tethering requires meiotic axis components (Red1/Hop1) and is modulated in a domain-specific fashion by cohesin. Loss of Rec114, Mer2 and Mei4 binding correlates with loss of DSBs. Our results strongly suggest that hotspot sequences become tethered to axis sites by the DSB machinery prior to DSB formation.
2011-08-28 | GSE29860 | GEO
Project description:We conducted a genome-wide expression analysis of wild-type males using three cell populations isolated from mitotic, meiotic and post-meiotic phases of spermatogenesis in Drosophila melanogaster. Our approach was to directly isolate testis regions enriched with RNAs from each of the three specific germline phases. We used microarrays to detail the global gene expression profile in spermatogenesis and identified up- and down-regulated genes between two different spermatogenic phases in pairwise comparisons Experiment Overall Design: Cell types present at various stages of spermatogenesis are generally located in a gradient along the proximal-distal axis of the testis, however most are not exclusively restricted to any one geographic region. Cells enriched for mitotic, meiotic and post-meiotic phases were obtained by dissection of apical, proximal and distal regions of the testis, respectively
2009-11-28 | E-GEOD-18502 | biostudies-arrayexpress
Project description:In most organisms, meiotic recombination begins with programmed DNA double strand break (DSB) formation by Spo11. Here, we present evidence that Tel1/Mec1, the budding yeast ATM/ATR, regulate DSB formation by phosphorylating Rec114, an essential Spo11-accessory protein. Analyses of a non-phosphorylatable- or phosphomimetic- alleles of rec114 revealed that DSB-dependent phosphorylation of Rec114 limited its association with DSB-hotspots resulting in reduction in DSB formation. Also observed were the impact of Rec114 phosphorylation on its homolog synapsis-associated removal from chromosomes and NDT80-dependent turnover. Specifically, we found that the synapsis- and NDT80-dependent Rec114 downregulation occurred later in the rec114 mutant with a reduced Spo11-catalysis, but earlier in the other with an enhanced catalysis, strongly implicating the existence of a feedback mechanism coupling the extent of Spo11-catalysis to Rec114 activity. Taken together, these observations suggest that three different mechanisms of down regulating Rec114 contribute to meiotic DSB homeostasis, a feedback mechanism to maintain the number of meiotic DSBs at the developmentally programmed level. 6 genome wide ChIPchip sets: 3 for meiotic DSB formation (Spo11-ChIP) and 3 for protein-DNA association (Rec114-ChIP), each for wild type and two mutants during meiosis (corresponding to the main Figure 3, as well as to Figures S3, S4, S5).
2013-06-01 | E-GEOD-43384 | biostudies-arrayexpress
Project description:In most organisms, meiotic recombination begins with programmed DNA double strand break (DSB) formation by Spo11. Here, we present evidence that Tel1/Mec1, the budding yeast ATM/ATR, regulate DSB formation by phosphorylating Rec114, an essential Spo11-accessory protein. Analyses of a non-phosphorylatable- or phosphomimetic- alleles of rec114 revealed that DSB-dependent phosphorylation of Rec114 limited its association with DSB-hotspots resulting in reduction in DSB formation. Also observed were the impact of Rec114 phosphorylation on its homolog synapsis-associated removal from chromosomes and NDT80-dependent turnover. Specifically, we found that the synapsis- and NDT80-dependent Rec114 downregulation occurred later in the rec114 mutant with a reduced Spo11-catalysis, but earlier in the other with an enhanced catalysis, strongly implicating the existence of a feedback mechanism coupling the extent of Spo11-catalysis to Rec114 activity. Taken together, these observations suggest that three different mechanisms of down regulating Rec114 contribute to meiotic DSB homeostasis, a feedback mechanism to maintain the number of meiotic DSBs at the developmentally programmed level.
2013-06-01 | GSE43384 | GEO
Project description:Human spermatogenesis is a well-ordered dynamic process, which ensures the long-term production of functional spermatozoa; however, the roles of DNA methylation and chromatin accessibility in this process remain largely unknown. Here, by simultaneously investigating the chromatin accessibility, DNA methylome and transcriptome landscapes of human spermatogenesis using the modified single-cell chromatin overall omic-scale landscape sequencing approach (Modified scCOOL-seq), we revealed that the transcriptional changes throughout human spermatogenesis were correlated with the dynamic alternations of chromatin accessibility; particularly, several potential transcription factors and a set of regulatory elements involved in such process were identified. Remarkably, a round of DNA demethylation was uncovered upon meiosis initiation in human spermatogenesis, which was associated with male meiotic recombination and conserved between human and mouse. And aberrant DNA hypermethylation at recombination hotspots could be detected in leptotene spermatocytes of certain nonobstructive azoospermia patients. Functionally, the intervention of DNA demethylation affected male meiotic recombination. Collectively, this study provides multi-omics landscapes of human spermatogenesis at single-cell resolution, and offers insights into the association between DNA demethylation and male meiotic recombination.
2023-07-09 | GSE235323 | GEO
Project description:Human spermatogenesis is a well-ordered dynamic process, which ensures the long-term production of functional spermatozoa; however, the roles of DNA methylation and chromatin accessibility in this process remain largely unknown. Here, by simultaneously investigating the chromatin accessibility, DNA methylome and transcriptome landscapes of human spermatogenesis using the modified single-cell chromatin overall omic-scale landscape sequencing approach (Modified scCOOL-seq), we revealed that the transcriptional changes throughout human spermatogenesis were correlated with the dynamic alternations of chromatin accessibility; particularly, several potential transcription factors and a set of regulatory elements involved in such process were identified. Remarkably, a round of DNA demethylation was uncovered upon meiosis initiation in human spermatogenesis, which was associated with male meiotic recombination and conserved between human and mouse. And aberrant DNA hypermethylation at recombination hotspots could be detected in leptotene spermatocytes of certain nonobstructive azoospermia patients. Functionally, the intervention of DNA demethylation affected male meiotic recombination. Collectively, this study provides multi-omics landscapes of human spermatogenesis at single-cell resolution, and offers insights into the association between DNA demethylation and male meiotic recombination.
2023-07-09 | GSE235322 | GEO