Similar Datasets
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
| PRJNA1029152 | ENA
Project description:DNA cytosine methylation suppresses meiotic recombination at the sex-determining region (ChiP-Seq)
| PRJNA1029155 | ENA
Project description:DNA cytosine methylation suppresses meiotic recombination at the sex-determining region (Bisulfite-Seq)
| PRJNA1029157 | ENA
Project description:DNA cytosine methylation suppresses meiotic recombination at the sex-determining region (RNA-Seq)
| PRJNA1029156 | ENA
Project description:DNA methylation is essential for protecting the mammalian germline against transposons. When DNA methylation-based transposon control is defective, meiotic chromosome pairing is consistently impaired during spermatogenesis: How and why meiosis is vulnerable to transposon activity is unknown. Using two DNA methylation-deficient backgrounds, the Dnmt3L and Miwi2 mutant mice, we reveal that DNA methylation is largely dispensable for silencing transposons before meiosis onset. After this, it becomes crucial to back up to a developmentally programmed H3K9me2 loss. Massive retrotransposition does not occur following transposon derepression, but the meiotic chromatin landscape is profoundly affected. Indeed, H3K4me3 marks gained over transcriptionally active transposons correlate with formation of SPO11-dependent double-strand breaks and recruitment of the DMC1 repair enzyme in Dnmt3L(-/-) meiotic cells, whereas these features are normally exclusive to meiotic recombination hot spots. Here, we demonstrate that DNA methylation restrains transposons from adopting chromatin characteristics amenable to meiotic recombination, which we propose prevents the occurrence of erratic chromosomal events.
| S-EPMC4495397 | biostudies-literature
Project description:Meiotic recombination forms crossovers important for proper chromosome segregation and offspring viability. This complex process involves many proteins acting at each of the multiple steps of recombination. Recombination initiates by formation of DNA double-strand breaks (DSBs), which in the several species examined occur with high frequency at special sites (DSB hotspots). In Schizosaccharomyces pombe, DSB hotspots are bound with high specificity and strongly activated by linear element (LinE) proteins Rec25, Rec27 and Mug20, which form colocalized nuclear foci with Rec10, essential for all DSB formation and recombination. Here, we test the hypothesis that the nuclear localization signal (NLS) of Rec10 is crucial for coordinated nuclear entry after forming a complex with other LinE proteins. In NLS mutants, all LinE proteins were abundant in the cytoplasm, not the nucleus; DSB formation and recombination were much reduced but not eliminated. Nuclear entry of limited amounts of Rec10, apparently small enough for passive nuclear entry, can account for residual recombination. LinE proteins are related to synaptonemal complex proteins of other species, suggesting that they also share an NLS, not yet identified, and undergo protein complex formation before nuclear entry.This article has an associated First Person interview with Mélody Wintrebert, joint first author of the paper.
| S-EPMC7929924 | biostudies-literature
Project description:Cytosine DNA methylation (CDM) is a stable epigenetic modification to the genome and a widespread regulatory process in living organisms that involves multicomponent molecular machines. Genome-wide cytosine methylation patterning participates in the epigenetic reprogramming of a cell, suggesting that the biological information contained within methylation positions may be amenable to decoding. Adaptation to a new cellular or organismal environment also implies the potential for genome-wide redistribution of CDM changes that will ensure the stability of DNA molecules. This raises the question of whether or not we would be able to sort out the regulatory methylation signals from the CDM background ("noise") induced by thermal fluctuations. Here, we propose a novel statistical and information thermodynamic description of the CDM changes to address the last question. The physical basis of our statistical mechanical model was evaluated in two respects: 1) the adherence to Landauer's principle, according to which molecular machines must dissipate a minimum energy ? = kBT ln2 at each logic operation, where kB is the Boltzmann constant, and T is the absolute temperature and 2) whether or not the binary stretch of methylation marks on the DNA molecule comprise a language of sorts, properly constrained by thermodynamic principles. The study was performed for genome-wide methylation data from 152 ecotypes and 40 trans-generational variations of Arabidopsis thaliana and 93 human tissues. The DNA persistence length, a basic mechanical property altered by CDM, was estimated with values from 39 to 66.9 nm. Classical methylome analysis can be retrieved by applying information thermodynamic modelling, which is able to discriminate signal from noise. Our finding suggests that the CDM signal comprises a language scheme properly constrained by molecular thermodynamic principles, which is part of an epigenomic communication system that obeys the same thermodynamic rules as do current human communication systems.
| S-EPMC4786201 | biostudies-literature