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BMPR1A-mediated BMP signalling ensures correct mitosis-to-meiosis transition in mouse fetal ovarian germ cells, in vivo

ABSTRACT: BMPR1A-mediated BMP signalling ensures correct mitosis-to-meiosis transition in mouse fetal ovarian germ cells, in vivo

PROVIDER: PRJNA1117811 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29217243_1.fastq.gz	Fastqsanger.gz
	SRR29217243_2.fastq.gz	Fastqsanger.gz
	SRR29217244_1.fastq.gz	Fastqsanger.gz
	SRR29217244_2.fastq.gz	Fastqsanger.gz
	SRR29217245_1.fastq.gz	Fastqsanger.gz

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BMPR1A-mediated BMP signalling ensures correct mitosis-to-meiosis transition in mouse fetal ovarian germ cells, in vivo

Project description:A successful mitosis-to-meiosis transition in germ cells is essential for fertility in sexually reproducing organisms. In mice and humans, it is established that STRA8 expression is critical for meiotic onset in both sexes. Here we show that BMP signalling is also essential, not for STRA8 induction but for correct meiotic progression in mouse fetal ovarian germ cells. Germ cell-specific deletion of Bmpr1a caused aberrant expression of meiotic, pluripotency, and cell cycle genes in E14.5 mouse fetal ovaries. Our results verify a role for BMP signalling in instructing germ cell meiosis in female mice in vivo, and shed light on the regulatory mechanisms underlying fetal germ cell development.

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Nuclear MTHFD2 secures centromere methylation, chromosome stability and correct mitosis progression

Project description:Subcellular compartmentalization of metabolic enzymes may elicit specific cellular functions by establishing a unique metabolic environment. Indeed, the nuclear translocation of certain metabolic enzymes is required for epigenetic regulation and gene expression control. Here, we reveal that, in cancer cells, the mitochondrial enzyme methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) localizes in the nucleus during the G2-M phase of the cell cycle to secure mitosis progression. Nuclear MTHFD2 interacts with proteins involved in mitosis regulation and centromere stability, including the methyltransferases KMT5A and DNMT3B. Loss of MTHFD2 induces centromere overexpression and severe methylation defects, and impedes correct mitosis completion. As a consequence, MTHFD2 deficient cells accumulate chromosomal aberrations arising from chromosome congression and segregation defects. Blocking the catalytic nuclear function of MTHFD2 recapitulates the phenotype observed in MTHFD2 deficient cells, attributing to nuclear MTHFD2 an enzymatic active role in controlling mitosis. Our discovery uncovers a nuclear moonlighting role for the cancer target MTHFD2, and emphasizes that cancer metabolism rewiring may encompass the relocation of metabolic enzymes to alternative subcellular compartments.

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Hormone-responsive Bmpr1a maintains myoepithelial integrity during pregnancy

Project description:Myoepithelial and luminal cells synergistically expand in the mammary gland during pregnancy, and this process is precisely governed by hormone-related signaling pathways. The BMP signaling pathway is now known to play crucial roles in all organ systems. However, the functions of BMP signaling in the mammary gland remain unclear. Here, we found that Bmpr1a is upregulated by hormone-induced Sp1 at pregnancy. Using a doxycycline (Dox)-inducible Bmpr1a conditional knockout mouse model, we demonstrated that loss of Bmpr1a results in compromised myoepithelial integrity, reduced mammary stem cells and precocious alveolar differentiation during pregnancy. Mechanistically, Bmpr1a regulates the expression of p63 and Slug, two key regulators of myoepithelial maintenance, through pSmad1/5-Smad4 complexes, and consequently activate P-cadherin during pregnancy. Collectively, these findings identify a novel role of BMP signaling in maintaining the identity of myoepithelial cells and suppressing precocious alveolar formation.

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