父母的经验通过调节前体miRNA的核出口来协调虫蛋的化同步
Ya Nan Zhu1,2, Jing He1, Jiawen Wang1
1State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China.
Nature communications
|May 21, 2024
概括
父母高种群密度会触发虫中的FOXN1激活PTBP1. 这调节miR-276,控制卵化同步和调解跨代效应.
科学领域:
- 昆虫学 昆虫学是一门学科.
- 发展生物学 发展生物学
- 遗传学 遗传学是一种遗传学.
背景情况:
- 父母的环境经验影响后代的表型可塑性.
- 在虫中,成年种群密度会影响蛋生产和化同步,这对于疫情的爆发至关重要.
- 父母向后代传输信号的分子机制在很大程度上是未知的.
研究的目的:
- 阐明介导人口密度对虫蛋化同步的跨代影响的分子途径.
- 确定关键的监管因素,涉及到父母向后代传输信号的关键因素.
主要方法:
- 研究了虫中转录因子叉头盒蛋白N1 (FOXN1) 和多胺管结合蛋白1 (Ptbp1) 的作用.
- 利用分子生物学技术分析微RNA-276 (miR-276) 的调节.
- 研究了Ptbp1,出口蛋白5 (XPO5) 和miR-276前核细胞质运输之间的相互作用.
主要成果:
- 高人口密度诱导FOXN1,激活虫中的Ptbp1.
- 该FOXN1-Ptbp1通路调节miR-276,控制卵化同步.
- Ptbp1通过XPO5促进了前miR-276核出口,增加了卵细胞中的miR-276水平.
- 这种机制在各种昆虫物种中得到保护,这表明一种通用途径.
结论:
- 一个涉及FOXN1,Ptbp1和miR-276的新型分子途径调解了父母人口密度对虫蛋化同步的跨代影响.
- 预米R-276的Ptbp1依赖的核出口是昆虫中父母效应的保存机制.
- 结果提供了关于表型可塑性和虫爆发动态调节的见解.
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