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Schlank orchestrates insect developmental transition by switching H3K27 acetylation to trimethylation in the prothoracic gland
Proceedings of the National Academy of Sciences of the United States of America ( IF 9.4 ) Pub Date : 2024-08-22 , DOI: 10.1073/pnas.2401861121
Dongqin Yuan 1, 2 , Xing Zhang 1, 2 , Yan Yang 1, 2 , Ling Wei 3 , Hao Li 1, 2 , Tujing Zhao 1, 2 , Mengge Guo 1, 2 , Zheng Li 1, 2 , Zhu Huang 1, 2 , Min Wang 1, 2 , Zongcai Dai 1, 2 , Peixin Li 1, 2 , Qingyou Xia 1, 2 , Wenliang Qian 1, 2 , Daojun Cheng 1, 2
Affiliation  

Insect developmental transitions are precisely coordinated by ecdysone and juvenile hormone (JH). We previously revealed that accumulated H3K27 trimethylation (H3K27me3) at the locus encoding JH signal transducer Hairy is involved in the larval–pupal transition in insects, but the underlying mechanism remains to be fully defined. Here, we show in Drosophila and Bombyx that Rpd3-mediated H3K27 deacetylation in the prothoracic gland during the last larval instar promotes ecdysone biosynthesis and the larval–pupal transition by enabling H3K27me3 accumulation at the Hairy locus to induce its transcriptional repression. Importantly, we find that the homeodomain transcription factor Schlank acts to switch active H3K27 acetylation (H3K27ac) to repressive H3K27me3 at the Hairy locus by directly binding to the Hairy promoter and then recruiting the histone deacetylase Rpd3 and the histone methyltransferase PRC2 component Su(z)12 through physical interactions. Moreover, Schlank inhibits Hairy transcription to facilitate the larval–pupal transition, and the Schlank signaling cascade is suppressed by JH but regulated in a positive feedback manner by ecdysone. Together, our data uncover that Schlank mediates epigenetic reprogramming of H3K27 modifications in hormone actions during insect developmental transition.

中文翻译:


Schlank 通过将前胸腺中的 H3K27 乙酰化转变为三甲基化来协调昆虫发育转变



昆虫的发育转变是由蜕皮激素和保幼激素(JH)精确协调的。我们之前揭示了编码 JH 信号转导器 Hairy 的位点处累积的 H3K27 三甲基化 (H3K27me3) 参与了昆虫的幼虫-蛹转变,但其潜在机制仍有待完全确定。在这里,我们在果蝇和家蚕中发现,在最后幼虫龄期间,Rpd3 介导的前胸腺中的 H3K27 脱乙酰化通过使 H3K27me3 在毛状位点积累来诱导其转录抑制,从而促进蜕皮激素生物合成和幼虫-蛹转变。重要的是,我们发现同源域转录因子 Schlank 通过直接与 Hairy 启动子结合,然后招募组蛋白脱乙酰酶 Rpd3 和组蛋白甲基转移酶 PRC2 成分 Su(z),将 Hairy 基因座上的活性 H3K27 乙酰化 (H3K27ac) 转变为抑制性 H3K27me3 12 通过身体互动。此外,Schlank 抑制毛状转录以促进幼虫-蛹转变,并且 Schlank 信号级联被 JH 抑制,但受蜕皮激素以正反馈方式调节。总之,我们的数据揭示了 Schlank 介导了昆虫发育转变过程中激素作用中 H3K27 修饰的表观遗传重编程。
更新日期:2024-08-22
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