H3K9 demethylation-mediated transcriptional activation is required for male meiosis in Arabidopsis thaliana
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ABSTRACT:
PROVIDER: PRJNA774291 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR16568839_1.fastq.gz | Fastqsanger.gz | |||
| SRR16568839_2.fastq.gz | Fastqsanger.gz | |||
| SRR16568840_1.fastq.gz | Fastqsanger.gz | |||
| SRR16568840_2.fastq.gz | Fastqsanger.gz | |||
| SRR16568841_1.fastq.gz | Fastqsanger.gz |
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Project description:Dimethylation at histone H3 lysine 9 (H3K9me2), a critical mark for heterochromatin formation and transcriptional silencing, is usually methylated at transposable elements and repetitive sequences but unmethylated at bodies of protein-coding genes. It is known that deposition of H3K9me2 is essential for proper prophase progression in both mammals and plants. Nevertheless, function of removing H3K9me2 for meiosis is unknown. In this study, we show that H3K9 demethylases, IBM1 and JMJ27, together regulate chromosome pairing and segregation in early meiosis, through protecting thousands of protein-coding genes from ectopic H3K9me2, including meiotic-essential genes. In addition to IBM1 and JMJ27, we also found that the cohesin complex cofactors Precocious Dissociation of Sisters 5 (PDS5s) regulate the expression of essential meiotic genes by interacting with H3K9 demethylases, acting downstream of H3K9 demethylation. Therefore, H3K9 demethylases and PDS5s coordinately regulate male meiosis through regulating the expression of meiotic-essential genes. These findings provide insights into a novel function of removing H3K9me2 for meiosis and deeper understanding of the H3K9 demethylation-mediated transcriptional activation pathway.
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Project description:H3K9 tri-methylation (H3K9me3) has emerging functions in gene regulation in addition to its accumulation on constitutive heterochromatin at pericentromeres. It remains a mystery why and how H3K9me3 is dynamically regulated in male meiosis. Here, we identify a novel and critical regulator of H3K9 methylation and spermatogenic heterochromatin organization: the germline-specific protein MCAF2 (ATF7IP2). We show that MCAF2 amasses on autosomal and X pericentric heterochromatin in male germ cells. On the sex chromosomes, which undergo meiotic sex chromosome inactivation (MSCI), the DNA damage response pathway recruits MCAF2 to X pericentric heterochromatin, where it facilitates the recruitment of SETDB1, a histone methyltransferase that catalyzes H3K9me3. In the absence of MCAF2, germ cells are arrested in meiotic prophase, and the mutant analyses revealed that MCAF2 is required for the maintenance of MSCI, and for global activation of autosomal genes and retrotransposon-derived loci in meiosis; this reveals a regulatory function for MCAF2 that is counterintuitive to its association with repressive H3K9me3. Taken together, we propose that MCAF2 is a downstream effector of the DDR pathway in meiosis that coordinates the organization of heterochromatin and gene regulation through the spatial regulation of SETDB1-mediated H3K9me3 deposition.
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Project description:MCAF2/ATF7IP2 directs meiosis-specific H3K9 methylation
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Project description:H3K9 tri-methylation (H3K9me3) plays emerging roles in gene regulation, beyond its accumulation on pericentric constitutive heterochromatin. It remains a mystery why and how H3K9me3 undergoes dynamic regulation in male meiosis. Here, we identify a novel, critical regulator of H3K9 methylation and spermatogenic heterochromatin organization: the germline-specific protein ATF7IP2 (MCAF2). We show that, in male meiosis, ATF7IP2 amasses on autosomal and X pericentric heterochromatin, spreads through the entirety of the sex chromosomes, and accumulates on thousands of autosomal promoters and retrotransposon loci. On the sex chromosomes, which undergo meiotic sex chromosome inactivation (MSCI), the DNA damage response pathway recruits ATF7IP2 to X pericentric heterochromatin, where it facilitates the recruitment of SETDB1, a histone methyltransferase that catalyzes H3K9me3. In the absence of ATF7IP2, male germ cells are arrested in meiotic prophase. Analyses of ATF7IP2-deficient meiosis reveal the protein’s essential roles in the maintenance of MSCI, suppression of retrotransposons, and global activation of autosomal genes. We propose that ATF7IP2 is a downstream effector of the DDR pathway in meiosis that coordinates the organization of heterochromatin and gene regulation through the spatial regulation of SETDB1-mediated H3K9me3 deposition. We performed gene expression analysis using data obtained from RNA-seq of Atf7ip2+/+ and Atf7ip2-/- pachytene spermatocytes.
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