spr-5;met-2 突变体后代的不育可能是由遗传的 H3K4 甲基化和种系转录改变引起的。

microPublication biology Pub Date : 2024-10-05 eCollection Date: 2024-01-01 DOI:10.17912/micropub.biology.001365
Jazmin Dozier, Mattie Villhauer, Brandon Carpenter
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引用次数: 0

摘要

在秀丽隐杆线虫组蛋白甲基化的母体重编程过程中,组蛋白去甲基化酶 SPR-5 会去除 H3K4me,随后组蛋白甲基转移酶 MET-2 会添加 H3K9me。母体中 SPR-5 和 MET-2 的缺失会导致后代出现不育等遗传表型。在这里,我们发现敲除 H3K4 甲基转移酶 SET-2 或 H3K36 甲基转移酶 MES-4 可以部分挽救 spr-5 ;met-2 突变体后代的生殖系,这表明遗传性不育可能是由遗传性 H3K4 甲基化和生殖系转录改变引起的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Sterility in the offspring of spr-5; met-2 mutants may be caused by inherited H3K4 methylation and altered germline transcription.

During maternal reprogramming of histone methylation in C. elegans , H3K4me is removed by the histone demethylase, SPR-5 , and H3K9me is subsequently added by the histone methyltransferase, MET-2 . Maternal loss of SPR-5 and MET-2 causes inherited phenotypes, such as sterility, in the progeny. Here, we find that knocking down either the H3K4 methyltransferase SET-2 or the H3K36 methyltransferase MES-4 partially rescues the germline in the progeny of spr-5 ; met-2 mutants, suggesting that the inherited sterility may be caused by inherited H3K4 methylation and altered germline transcription.

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