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The H3K9 methyltransferase SETDB1 maintains female identity in Drosophila germ cells.
Nature Communications ( IF 14.7 ) Pub Date : 2018-10-08 , DOI: 10.1038/s41467-018-06697-x
Anne E. Smolko , Laura Shapiro-Kulnane , Helen K. Salz

The preservation of germ cell sexual identity is essential for gametogenesis. Here we show that H3K9me3-mediated gene silencing is integral to female fate maintenance in Drosophila germ cells. Germ cell specific loss of the H3K9me3 pathway members, the H3K9 methyltransferase SETDB1, WDE, and HP1a, leads to ectopic expression of genes, many of which are normally expressed in testis. SETDB1 controls the accumulation of H3K9me3 over a subset of these genes without spreading into neighboring loci. At phf7, a regulator of male germ cell sexual fate, the H3K9me3 peak falls over the silenced testis-specific transcription start site. Furthermore, H3K9me3 recruitment to phf7 and repression of testis-specific transcription is dependent on the female sex determination gene Sxl. Thus, female identity is secured by an H3K9me3 epigenetic pathway in which Sxl is the upstream female-specific regulator, SETDB1 is the required chromatin writer, and phf7 is one of the critical SETDB1 target genes.

中文翻译:

H3K9甲基转移酶SETDB1在果蝇生殖细胞中保持女性身份。

保留生殖细胞的性身份对于配子发生至关重要。在这里,我们显示H3K9me3介导的基因沉默是果蝇生殖细胞中女性命运维持所必需的。H3K9me3途径成员H3K9甲基转移酶SETDB1,WDE和HP1a的生殖细胞特异性损失导致异位表达基因,其中许多通常在睾丸中表达。SETDB1控制H3K9me3在这些基因的一个子集上的积累,而不会扩散到邻近的基因座中。在phf7(雄性生殖细胞性命运的调节者)处,H3K9me3峰落在沉默的睾丸特异性转录起始位点上。此外,H3K9me3募集到phf7和睾丸特异性转录的抑制取决于女性性别决定基因Sxl。因此,
更新日期:2018-10-08
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