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The EGR family gene egrh-1 functions non-autonomously in the control of oocyte meiotic maturation and ovulation in C. elegans

机译:EGR家族基因egrh-1在控制秀丽隐杆线虫的卵母细胞减数分裂成熟和排卵中非自主地起作用

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摘要

Oocyte production, maturation and ovulation must be coordinated with sperm availability for successful fertilization. In C. elegans this coordination involves signals from the sperm to the oocyte and somatic gonad, which stimulate maturation and ovulation. We have found that the C. elegans early growth response factor family member EGRH-1 inhibits oocyte maturation and ovulation until sperm are available. In the absence of sperm, egrh-1 mutants exhibit derepressed oocyte maturation marked by MAPK activation and ovulation. egrh-1 mutants exhibit ectopic oocyte differentiation in the distal gonadal arm and accumulate abnormal and degraded oocytes proximally. These defects result in reduced brood size and partially penetrant embryonic lethality. We have found that endogenous EGRH-1 protein and an egrh-1::gfp reporter gene are expressed in the sheath and distal tip cells of the somatic gonad, the gut and other non-gonadal tissues, as well as in sperm, but expression is not observed in oocytes. Results of tissue-specific egrh-1(RNAi) experiments and genetic mosaic analyses revealed that EGRH-1 function is necessary in the soma and, surprisingly, this function is required in both the gut and the somatic gonad. Based on transformation rescue experiments we hypothesize that EGRH-1 in the somatic gonad inhibits oocyte maturation and ovulation.
机译:卵母细胞的生产,成熟和排卵必须与精子的可利用性相协调才能成功受精。在秀丽隐杆线虫中,这种协调涉及从精子到卵母细胞和体细胞性腺的信号,这些信号刺激成熟和排卵。我们已经发现线虫的早期生长反应因子家族成员EGRH-1抑制卵母细胞的成熟和排卵,直到精子可用。在没有精子的情况下,egrh-1突变体表现出受抑制的卵母细胞成熟,其特征在于MAPK激活和排卵。 egrh-1突变体在远端性腺臂中表现出异位卵母细胞分化,并在近端积累异常和降解的卵母细胞。这些缺陷导致育雏尺寸减小和部分渗透性胚胎致死率。我们已经发现内源性EGRH-1蛋白和egrh-1 :: gfp报告基因在体细胞性腺,肠和其他非性腺组织以及精子的鞘和末梢细胞中表达,但表达在卵母细胞中未观察到。组织特异性egrh-1(RNAi)实验和遗传镶嵌分析的结果表明,EGRH-1功能在躯体中是必需的,令人惊讶的是,肠道和体细胞性腺都需要该功能。基于转化拯救实验,我们假设体细胞性腺中的EGRH-1抑制卵母细胞的成熟和排卵。

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