PDF(Pubmed)
Abstract：
Parental experiences can affect the phenotypic plasticity of offspring. In locusts, the population density that adults experience regulates the number and hatching synchrony of their eggs, contributing to locust outbreaks. However, the pathway of signal transmission from parents to offspring remains unclear. Here, we find that transcription factor Forkhead box protein N1 (FOXN1) responds to high population density and activates the polypyrimidine tract-binding protein 1 (Ptbp1) in locusts. FOXN1-PTBP1 serves as an upstream regulator of miR-276, a miRNA to control egg-hatching synchrony. PTBP1 boosts the nucleo-cytoplasmic transport of pre-miR-276 in a \"CU motif\"-dependent manner, by collaborating with the primary exportin protein exportin 5 (XPO5). Enhanced nuclear export of pre-miR-276 elevates miR-276 expression in terminal oocytes, where FOXN1 activates Ptbp1 and leads to egg-hatching synchrony in response to high population density. Additionally, PTBP1-prompted nuclear export of pre-miR-276 is conserved in insects, implying a ubiquitous mechanism to mediate transgenerational effects.
摘要：
父母经历会影响后代的表型可塑性。在蝗虫中,成年人经历的人口密度调节卵的数量和孵化同步性，导致蝗虫爆发。然而,从父母到后代的信号传递途径仍不清楚。这里,我们发现转录因子Forkheadbox蛋白N1（FOXN1）响应高种群密度并激活蝗虫中的聚嘧啶束结合蛋白1（Ptbp1）。FOXN1-PTBP1作为miR-276的上游调节因子，miR-276是一种控制卵孵化同步性的miRNA。PTBP1以“CU基序”依赖性方式增强前miR-276的核质转运，通过与初级输出蛋白输出蛋白5(XPO5)合作。前miR-276的核输出增强提高了末端卵母细胞中miR-276的表达,其中FOXN1激活Ptbp1并导致卵孵化同步，以响应高人口密度。此外,PTBP1提示的pre-miR-276的核输出在昆虫中是保守的，暗示了一种无处不在的机制来介导跨代效应。
