LSM1-mediated Major Satellite RNA decay is required for nonequilibrium histone H3.3 incorporation into parental pronuclei.
LSM1-mediated Major Satellite RNA decay is required for nonequilibrium histone H3.3 incorporation into parental pronuclei.
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LSM1 介导的主要卫星 RNA 衰变是非平衡组蛋白 H3.3 掺入亲本原核所必需的
DOI：
10.1038/s41467-023-36584-z
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发表时间：
2023-02-21
影响因子：
16.6
通讯作者：
Kang, Lan
中科院分区：
文献类型：
--
作者：
Zhu, Jiang;Chen, Kang;Sun, Yu H.;Ye, Wen;Liu, Juntao;Zhang, Dandan;Su, Nan;Wu, Li;Kou, Xiaochen;Zhao, Yanhong;Wang, Hong;Gao, Shaorong;Kang, Lan
在哺乳动物中，亲本基因组的表观遗传重编程对于合子基因组激活和随后的胚胎发育是必不可少的。以前已经观察到组蛋白H3变异体不对称地整合到亲本基因组中，但潜在的机制仍然难以捉摸。在本研究中，我们发现RNA结合蛋白LSM1介导的主要卫星RNA衰变在组蛋白变异体H3.3优先掺入雄性原核中起核心作用。Lsm1的敲除破坏了非平衡原核的组蛋白掺入和不对称的H3K9me3修饰。随后，我们发现LSM1主要针对主要卫星重复RNA(MajSat RNA)进行衰变，并且在Lsm1缺失的卵母细胞中积累的MajSat RNA导致H3.1异常掺入雄性原核。MajSat RNA的敲除逆转了Lsm1敲除受精卵中组蛋白的异常掺入和修饰。因此，我们的研究揭示了亲本原核中组蛋白变体的准确掺入和附带修饰是由依赖于LSM1的着丝粒周围RNA衰变所指定的。
Epigenetic reprogramming of the parental genome is essential for zygotic genome activation and subsequent embryo development in mammals. Asymmetric incorporation of histone H3 variants into the parental genome has been observed previously, but the underlying mechanism remains elusive. In this study, we discover that RNA-binding protein LSM1-mediated major satellite RNA decay plays a central role in the preferential incorporation of histone variant H3.3 into the male pronucleus. Knockdown of Lsm1 disrupts nonequilibrium pronucleus histone incorporation and asymmetric H3K9me3 modification. Subsequently, we find that LSM1 mainly targets major satellite repeat RNA (MajSat RNA) for decay and that accumulated MajSat RNA in Lsm1-depleted oocytes leads to abnormal incorporation of H3.1 into the male pronucleus. Knockdown of MajSat RNA reverses the anomalous histone incorporation and modifications in Lsm1-knockdown zygotes. Our study therefore reveals that accurate histone variant incorporation and incidental modifications in parental pronuclei are specified by LSM1-dependent pericentromeric RNA decay.
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