A miR-590/Acvr2a/Rad51b Axis Regulates DNA Damage Repair during mESC Proliferation

A miR-590/Acvr2a/Rad51b Axis Regulates DNA Damage Repair during mESC Proliferation

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Embryonic stem cells (ESCs) enable rapid proliferation that also causes DNA damage.To maintain genomic stabilization during Fruit / Vegetable Wedgers rapid proliferation, ESCs must have an efficient system to repress genotoxic stress.Here, we show that withdrawal of leukemia inhibitory factor (LIF), which maintains the self-renewal capability of mouse ESCs (mESCs), significantly inhibits the cell proliferation and DNA damage of mESCs and upregulates the expression of miR-590.miR-590 promotes single-strand break (SSB) and double-strand break (DSB) damage repair, thus slowing proliferation of mESCs without influencing stemness.

miR-590 directly targets Activin receptor type 2a (Acvr2a) to mediate Activin signaling.We identified the homologous recombination-mediated repair (HRR) gene, Rad51b, as a downstream molecule of the miR-590/Acvr2a pathway regulating the SSB and DSB COMPASS damage repair and cell cycle.Our study shows that a miR-590/Acvr2a/Rad51b signaling axis ensures the stabilization of mESCs by balancing DNA damage repair and rapid proliferation during self-renewal.