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The S. cerevisiae m6A reader Pho92 impacts meiotic recombination by controlling key methylated transcripts [RNA-seq]

ABSTRACT: The S. cerevisiae m6A reader Pho92 impacts meiotic recombination by controlling key methylated transcripts [RNA-seq]

PROVIDER: PRJNA822917 | ENA |

REPOSITORIES: ENA

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The S. cerevisiae m6A reader Pho92 impacts meiotic recombination by controlling key methylated transcripts.

Project description:The S. cerevisiae m6A reader Pho92 impacts meiotic recombination by controlling key methylated transcripts.

| PRJNA822912 | ENA

The S. cerevisiae m6A reader Pho92 impacts meiotic recombination by controlling key methylated transcripts [CRAC]

Project description:The S. cerevisiae m6A reader Pho92 impacts meiotic recombination by controlling key methylated transcripts [CRAC]

| PRJNA822916 | ENA

The S. cerevisiae m6A reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts [RNA-seq]

Project description:We performed high-throughput mRNA sequencing during a meiotic time course (0, 2, 3, 5, 6, 7 and 9 hr) in WT, pho92 mutant and ime4 mutant cells.

2022-07-08 | GSE200087 | GEO

The S. cerevisiae m6A reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts.

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-08 | GSE200089 | GEO

The S. cerevisiae m6A reader Pho92 promotes timely meiotic recombination by controlling key methylated transcripts [CRAC]

Project description:We performed CRAC (UV-crosslinking and analysis of cDNA) to identify Ime4-dependent mRNA targets of Pho92 during meiosis at 5 hr in SPO.

2022-07-08 | GSE200088 | GEO

Dual Histone Methyl Reader ZCWPW1 Facilitates Repair of PRDM9-Induced Meiotic Double Strand Breaks

Project description:Meiotic crossovers result from homology-directed repair of double strand breaks (DSBs). Unlike yeast and plants, where DSBs are generated near gene promoters, in many vertebrates, DSBs are enriched at hotspots determined by the DNA binding activity of the rapidly evolving zinc finger array of PRDM9 (PR domain zinc finger protein 9), which subsequently catalyzes trimethylation of lysine 4 and lysine 36 of Histone H3 in nearby nucleosomes. Here, we identify the dual histone methylation reader ZCWPW1, which is tightly co-expressed during spermatogenesis with Prdm9 and co-evolved with Prdm9 in vertebrates, as an essential meiotic recombination factor required for efficient synapsis and repair of PRDM9-dependent DSBs. In sum, our results indicate that the evolution of dual histone methylation reader/writer system involving Prdm9 and Zcwpw1 facilitated a shift in genetic recombination away from a static pattern near genes towards a flexible pattern controlled by the rapidly evolving DNA binding activity of PRDM9

2020-05-12 | GSE139289 | GEO

Meiotic recombination cold spots in chromosomal cohesion sites [ChIP-Seq]

Project description:Meiotic chromosome architecture called M-bM-^@M-^\axis-loop structuresM-bM-^@M-^] and histone modifications have been demonstrated to regulate the Spo11-dependent formation of DNA double-strand breaks (DSBs) that trigger meiotic recombination. Using genome-wide chromatin immunoprecipitation (ChIP) analyses followed by deep sequencing, we compared the genome-wide distribution of the axis protein Rec8 (the kleisin subunit of meiotic cohesin) with that of oligomeric DNA covalently bound to Spo11, indicative of DSB sites. The frequency of DSB sites is overall constant between Rec8 binding sites. However, DSB cold spots are observed in regions spanning M-BM-10.8 kb around Rec8 binding sites. The axis-associated cold spots are not due to exclusion of Spo11 localization from the axis, since ChIP experiments revealed that substantial Spo11 persists at Rec8 binding sites during DSB formation. Spo11 fused with Gal4 DNA binding domain (Gal4BD-Spo11) tethered in close proximity (M-bM-^IM-$0.8 kb) to Rec8 binding sites hardly forms meiotic DSBs, in contrast with other regions. In addition, H3K4 tri-methylation (H3K4me3) remarkably decreases at Rec8 binding sites. These results suggest that reduced histone H3K4me3 in combination with inactivation of Spo11 activity on the axis discourages DSB hot spot formation. ChIP-seq analyses of Rec8, Spo11, and Gal4BD-Spo11 on budding yeast meiotic chromosomes M-bM-^@M-" Distribution of Rec8 in wt and Gal4BD-Spo11-expressing cells at 4h after meiotic induction M-bM-^@M-" Distribution of Spo11 at 3h, 4h, and 5h after meiotic induction M-bM-^@M-" Distribution of Gal4BD-Spo11 at 0h after meiotic induction

2014-03-31 | E-GEOD-52862 | biostudies-arrayexpress

Structural basis of YTH domain as m6A reader

Project description:The N6-methyladenosine (m6A) is the most abundant internal modification in almost all eukaryotic messenger RNAs, and is dynamically regulated. Therefore, identification of m6A readers is especially important in determining the cellular function of m6A. YTHDF2 has recently been characterized as the first m6A reader that regulates the cytoplasmic stability of methylated RNA. Here we show that YTHDC1 is a nuclear m6A reader and report the crystal structure of the YTH domain of YTHDC1 bound to m6A-containing RNA. We further determined the structure of another YTH domain, YTHDF1, and found that the YTH domain utilizes a conserved aromatic cage to specifically recognize the methyl group of m6A. Our structural characterizations of the YTHDC1-m6A RNA complex also shed light on the molecular basis for the preferential binding of the GG(m6A)C sequence by YTHDC1 and confirm the YTH domain as a specific m6A RNA reader. PAR-CLIP (Photoactivatable-Ribonucleoside-Enhanced Crosslinking and Immunoprecipitation) was applied to human YTHDC1 protein to identify its binding sites.

2014-09-18 | E-GEOD-58352 | biostudies-arrayexpress

Principles of chromosome organization for meiotic recombination

Project description:In meiotic cells, chromosomes are organized as chromatin loop arrays anchored to a protein axis. This organization is essential to regulate meiotic recombination, from DNA double-strand break (DSB) formation to their repair. In mammals, it is unknown how chromatin loops are organized along the genome and how proteins participating in DSB formation are tethered to the chromosome axes. Here, we identified three categories of axis-associated genomic sites: PRDM9 binding sites, where DSBs form, binding sites of the insulator protein CTCF, and H3K4me3-enriched sites. We demonstrated that PRDM9 promotes the recruitment of MEI4 and IHO1, two proteins essential for DSB formation. In turn, IHO1 anchors DSB sites to the axis components HORMAD1 and SYCP3. We discovered that IHO1, HORMAD1 and SYCP3 are associated at the DSB ends during DSB repair. Our results highlight how interactions of proteins with specific genomic elements shape the meiotic chromosome organization for recombination.

2024-04-23 | GSE262343 | GEO

Chromatin binding by HORMAD proteins regulates meiotic recombination initiation

Project description:The meiotic chromosome axis coordinates chromosome organization and interhomolog recombination in meiotic prophase, and is essential for fertility. In S. cerevisiae, the HORMAD protein Hop1 mediates an enrichment of axis proteins at nucleosome-rich genomic islands through a central chromatin-binding region (CBR). Here, we use cryoelectron microscopy to show that the Hop1 CBR directly recognizes bent nucleosomal DNA through a composite interface in its PHD and winged helix-turn-helix domains. Targeted disruption of the Hop1 CBR-nucleosome interface causes a loss of axis-protein enrichment at nucleosome-rich genomic islands, reduces meiotic DNA double-strand breaks (DSBs), and causes defects in chromosome synapsis. Synthetic effects with the disassemblase Pch2 suggest that nucleosome binding delays a conformational switch in Hop1 from a DSB-promoting, Pch2-inaccessible state to a DSB-inactive, Pch2-accessible state to regulate the extent of meiotic DSB formation . Phylogenetic analyses of meiotic HORMADs reveal an ancient origin of this domain, suggesting that these mechanisms are broadly conserved.

2024-02-28 | GSE225129 | GEO

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