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Actin depolymerization is associated with meiotic acceleration in cycloheximide-treated ovine oocytes

机译:肌动蛋白解聚与环己酰亚胺治疗的绵羊卵母细胞减数分裂加速有关

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摘要

Oocytes treated with the protein synthesis inhibitor cycloheximide (CHX) arrest at the germinal vesicle (GV) stage and undergo accelerated GV breakdown (GVBD) after CHX is removed. However, little is known about the underlying mechanism of accelerated meiotic maturation. Here, we investigated this mechanism and found that oocytes released from CHX arrest have higher amounts of cyclin B1 (CCNB1) and phosphorylated mitogen-activated protein kinase (pMAPK) proteins. Increased levels of these factors were not associated with mRNA polyadenylation or increased transcription rates of CCNB1 and MOS (Moloney murine sarcoma viral oncogene homolog) during CHX arrest. We found that treatment of CHX-arrested oocytes with the actin filament-stabilizing agent Jasplakinolide (Jasp) delayed GVBD following release from CHX arrest and that this was correlated with reduced maturation-promoting factor (MPF) activity. These results suggest that CCNB1 mRNAs released from actin filaments during CHX arrest increase CCNB1 transcripts available for translation after release from CHX arrest, leading to the precocious activation of MPF and accelerated meiotic progression.
机译:用蛋白质合成抑制剂环己酰亚胺(CHX)处理的卵母细胞在生小泡(GV)阶段停滞,并在去除CHX后经历加速的GV分解(GVBD)。但是,对减数分裂加速成熟的潜在机制知之甚少。在这里,我们研究了这种机制,发现从CHX逮捕释放的卵母细胞中细胞周期蛋白B1(CCNB1)和磷酸化的丝裂原活化蛋白激酶(pMAPK)蛋白含量更高。在CHX逮捕期间,这些因子水平的增加与mRNA多聚腺苷酸化或CCNB1和MOS(莫洛尼鼠肉瘤病毒癌基因同源物)的转录率增加无关。我们发现,用肌动蛋白丝稳定剂Jasplakinolide(Jasp)处理CHX停滞的卵母细胞会延迟从CHX释放释放的GVBD,这与降低的成熟促进因子(MPF)活性有关。这些结果表明在CHX停止期间从肌动蛋白丝释放的CCNB1 mRNA增加了CHNB停止释放后可用于翻译的CCNB1转录本,导致MPF的早熟激活和减数分裂进程的加速。

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