DNA cytosine methylation suppresses meiotic recombination at the sex-determining region (ChiP-Seq)
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PROVIDER: PRJNA1029155 | ENA |
REPOSITORIES: ENA
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Project description:DNA cytosine methylation suppresses meiotic recombination at the sex-determining region
| PRJNA1029152 | ENA
Project description:In sexual organisms, random meiotic recombination between homologous chromosomes is vital to maximize genetic variation among offspring. The sex-determining region (SDR), however, does not undergo recombination, as required for the maintenance of distinct alleles. The contribution of epigenetic versus genetic mechanisms to suppress recombination in SDRs and how the suppression mechanisms evolve remain poorly understood. Here we describe the mechanistic control of meiotic recombination at the mating-type locus (MT) in the green alga Chlamydomonas reinhardtii. We identify a maintenance DNA methyltransferase, DNMT1, mutation of which leads to the depletion of 95% of 5-methylcytosines (5mCs) in the nuclear genome. While the 5mC deficiency causes no discernible alteration in haploid vegetative growth or sexual differentiation, the dnmt1 homozygotes display substantially reduced spore viability and 4-progeny-tetrad frequency. Strikingly, in dnmt1 homozygotes, anomalous meiotic recombination takes place at MT, generating haploid progenies with mixed mating-type harboring both plus and minus markers. Although the repressive histone methylation H3K9me1 at MT is lost concurrently in dnmt1 strains, loss of histone methylation alone by gene deletion of the responsible histone methyltransferase SET3p does not lead to anomalous recombination at MT. Thus, DNA methylation, rather than histone modification, mediates the recombination suppression at MT in C. reinhardtii. This finding suggests that in early eukaryotes, which likely lacked histone-based chromatin modification, DNA methylation may have been co-opted to suppress meiotic recombination between alleles responsible for separate sexes.
2024-08-20 | GSE245613 | GEO
Project description:In sexual organisms, random meiotic recombination between homologous chromosomes is vital to maximize genetic variation among offspring. The sex-determining region (SDR), however, does not undergo recombination, as required for the maintenance of distinct alleles. The contribution of epigenetic versus genetic mechanisms to suppress recombination in SDRs and how the suppression mechanisms evolve remain poorly understood. Here we describe the mechanistic control of meiotic recombination at the mating-type locus (MT) in the green alga Chlamydomonas reinhardtii. We identify a maintenance DNA methyltransferase, DNMT1, mutation of which leads to the depletion of 95% of 5-methylcytosines (5mCs) in the nuclear genome. While the 5mC deficiency causes no discernible alteration in haploid vegetative growth or sexual differentiation, the dnmt1 homozygotes display substantially reduced spore viability and 4-progeny-tetrad frequency. Strikingly, in dnmt1 homozygotes, anomalous meiotic recombination takes place at MT, generating haploid progenies with mixed mating-type harboring both plus and minus markers. Although the repressive histone methylation H3K9me1 at MT is lost concurrently in dnmt1 strains, loss of histone methylation alone by gene deletion of the responsible histone methyltransferase SET3p does not lead to anomalous recombination at MT. Thus, DNA methylation, rather than histone modification, mediates the recombination suppression at MT in C. reinhardtii. This finding suggests that in early eukaryotes, which likely lacked histone-based chromatin modification, DNA methylation may have been co-opted to suppress meiotic recombination between alleles responsible for separate sexes.
2024-08-20 | GSE245612 | GEO
Project description:In sexual organisms, random meiotic recombination between homologous chromosomes is vital to maximize genetic variation among offspring. The sex-determining region (SDR), however, does not undergo recombination, as required for the maintenance of distinct alleles. The contribution of epigenetic versus genetic mechanisms to suppress recombination in SDRs and how the suppression mechanisms evolve remain poorly understood. Here we describe the mechanistic control of meiotic recombination at the mating-type locus (MT) in the green alga Chlamydomonas reinhardtii. We identify a maintenance DNA methyltransferase, DNMT1, mutation of which leads to the depletion of 95% of 5-methylcytosines (5mCs) in the nuclear genome. While the 5mC deficiency causes no discernible alteration in haploid vegetative growth or sexual differentiation, the dnmt1 homozygotes display substantially reduced spore viability and 4-progeny-tetrad frequency. Strikingly, in dnmt1 homozygotes, anomalous meiotic recombination takes place at MT, generating haploid progenies with mixed mating-type harboring both plus and minus markers. Although the repressive histone methylation H3K9me1 at MT is lost concurrently in dnmt1 strains, loss of histone methylation alone by gene deletion of the responsible histone methyltransferase SET3p does not lead to anomalous recombination at MT. Thus, DNA methylation, rather than histone modification, mediates the recombination suppression at MT in C. reinhardtii. This finding suggests that in early eukaryotes, which likely lacked histone-based chromatin modification, DNA methylation may have been co-opted to suppress meiotic recombination between alleles responsible for separate sexes.
2024-08-20 | GSE245611 | GEO
Project description:DNA cytosine methylation suppresses meiotic recombination at the sex-determining region (RNA-Seq)
| PRJNA1029156 | ENA
Project description:DNA cytosine methylation suppresses meiotic recombination at the sex-determining region (Bisulfite-Seq)
| PRJNA1029157 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-08-20 | GSE245614 | GEO
Project description:Meiotic recombination differs between males and females, however, when and how these differences are established is unknown. We identify extensive sex differences at recombination initiation by mapping hotspots of meiotic DNA double strand breaks in male and female mice. Contrary to past findings in humans, few hotspots are used uniquely in either sex. Instead, grossly different recombination landscapes result from up to 15-fold differences in hotspot use between males and females. Indeed, most recombination occurs at sex-biased hotspots. Sex biased hotspots appear to be partly determined by chromosome structure, and DNA methylation, absent in females at the onset of meiosis, plays a substantial role. Sex differences are also evident later in meiosis as the repair frequency of distal meiotic breaks as crossovers diverges in males and females. Suppression of distal crossovers may help to minimize age-related aneuploidy that arises due to cohesion loss during dictyate arrest in females.
2018-09-20 | GSE99921 | GEO
Project description:Orderly segregation of chromosomes during meiosis requires that crossovers form between homologous chromosomes by recombination. Programmed DNA double-strand breaks (DSBs) initiate meiotic recombination. We identify ANKRD31 as a critical component of complexes of DSB-promoting proteins which assemble on meiotic chromosome axes. Genome-wide, ANKRD31 deficiency causes delayed recombination initiation. In addition, loss of ANKRD31 alters DSB distribution owing to reduced selectivity for sites that normally attract DSBs. Strikingly, ANKRD31 deficiency also abolishes uniquely high rates of recombination that normally characterize pseudoautosomal regions (PARs) of X and Y chromosomes. Consequently, sex chromosomes do not form crossovers leading to chromosome segregation failure in ANKRD31-deficient spermatocytes. These defects are accompanied by a genome-wide delay in assembling DSB-promoting proteins on axes and a loss of a pecialized PAR-axis domain that is highly enriched for DSB-promoting proteins. Thus, we propose a model for spatiotemporal patterning of recombination by ANKRD31-dependent control of axis-associated complexes of DSB-promoting proteins.
2019-06-07 | GSE126443 | GEO
Project description:Temperature is key for biological activities, but its role in meiotic recombination processes is less known. Here, we uncovered the patterns of meiotic recombination by monitoring the double strands DNA breaks in diploid strain ZK5 cells cultured at 14ºC, 30ºC, and 37ºC.
2017-07-04 | GSE100741 | GEO