Brown Hannah E, Varderesian Haik V, Keane Sara A, Ryder Sean P
bioRxiv. 2025 Feb 20:2024.04.01.587367. doi: 10.1101/2024.04.01.587367.
Organisms must sense temperature and modify their physiology to survive environmental stress. Elevated temperature reduces fertility in most sexually reproducing organisms. Maternally supplied mRNAs are required for embryogenesis. They encode proteins that govern early embryonic patterning. RNA-binding proteins (RBPs) are major effectors of maternal mRNA regulation. MEX-3 is a conserved RBP essential for anterior patterning of embryos. We previously demonstrated that the 3' untranslated region (3'UTR) represses MEX-3 abundance in the germline yet is mostly dispensable for fertility. Here, we show that the 3'UTR is essential during thermal stress. Deletion of the 3'UTR causes a highly penetrant temperature sensitive embryonic lethality phenotype distinct from a null. Loss of the 3'UTR decreases MEX-3 abundance specifically in maturing oocytes and early embryos during temperature stress. Dysregulation of reprograms the thermal stress response by reducing the expression of hundreds of heat shock genes. We propose that the primary role of the 3'UTR is to buffer MEX-3 expression during fluctuating temperature, ensuring the robustness of oocyte maturation and embryogenesis.
生物体必须感知温度并调节其生理机能以在环境压力下生存。高温会降低大多数有性生殖生物体的生育能力。胚胎发育需要母源提供的mRNA。它们编码调控早期胚胎模式形成的蛋白质。RNA结合蛋白(RBPs)是母源mRNA调控的主要效应因子。MEX-3是一种保守的RBP,对胚胎的前部模式形成至关重要。我们之前证明,3'非翻译区(3'UTR)在生殖系中抑制MEX-3的丰度,但对生育能力大多是可有可无的。在此,我们表明3'UTR在热应激期间至关重要。删除3'UTR会导致一种高度显性的温度敏感型胚胎致死表型,与缺失型不同。3'UTR的缺失会在温度应激期间特异性地降低成熟卵母细胞和早期胚胎中MEX-3的丰度。MEX-3失调通过降低数百个热休克基因的表达来重新编程热应激反应。我们提出,3'UTR的主要作用是在温度波动期间缓冲MEX-3的表达,确保卵母细胞成熟和胚胎发育的稳健性。