Ontology highlight
ABSTRACT:
PROVIDER: PRJEB27323 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR2641190_1.fastq.gz | Fastqsanger.gz | |||
| ERR2641190_2.fastq.gz | Fastqsanger.gz | |||
| ERR2641191_1.fastq.gz | Fastqsanger.gz | |||
| ERR2641191_2.fastq.gz | Fastqsanger.gz | |||
| ERR2641182_1.fastq.gz | Fastqsanger.gz |
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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.
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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.
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Project description:Systems analysis reveals that Chlamydomonas reinhardtii responds rapidly and flexibly to an increase in light intensity. Rising metabolite levels and post-translation regulation facilitate a rapid increase in the rate of carbon fixation and a slightly delayed increase in the rate of growth, and slower changes in protein abundance adjust allocation and minimize bottlenecks in the new conditions.
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