Department of Biology, The Johns Hopkins University, Baltimore, MD, 21218, USA.
Laboratory of Chromatin Biology and Epigenetics, The Rockefeller University, New York, NY, 10065, USA.
Cell Death Differ. 2018 Aug;25(8):1486-1502. doi: 10.1038/s41418-017-0056-5. Epub 2018 Jan 23.
Tissue homeostasis depends on the ability of tissue-specific adult stem cells to maintain a balance between proliferation and differentiation, as well as ensure DNA damage repair. Here, we use the Drosophila male germline stem cell system to study how a chromatin factor, enhancer of polycomb [E(Pc)], regulates the proliferation-to-differentiation (mitosis-to-meiosis) transition and DNA damage repair. We identified two critical targets of E(Pc). First, E(Pc) represses CycB transcription, likely through modulating H4 acetylation. Second, E(Pc) is required for accumulation of an important germline differentiation factor, Bag-of-marbles (Bam), through post-transcriptional regulation. When E(Pc) is downregulated, increased CycB and decreased Bam are both responsible for defective mitosis-to-meiosis transition in the germline. Moreover, DNA double-strand breaks (DSBs) accumulate upon germline inactivation of E(Pc) under both physiological condition and recovery from heat shock-induced endonuclease expression. Failure of robust DSB repair likely leads to germ cell loss. Finally, compromising the activity of Tip60, a histone acetyltransferase, leads to germline defects similar to E(Pc) loss-of-function, suggesting that E(Pc) acts cooperatively with Tip60. Together, our data demonstrate that E(Pc) has pleiotropic roles in maintaining male germline activity and genome integrity. Our findings will help elucidate the in vivo molecular mechanisms of E(Pc).
组织稳态依赖于组织特异性成体干细胞在增殖和分化之间保持平衡的能力,以及确保 DNA 损伤修复的能力。在这里,我们使用果蝇雄性生殖干细胞系统来研究染色质因子增强子多梳 [E(Pc)] 如何调节增殖到分化(有丝分裂到减数分裂)的转变和 DNA 损伤修复。我们鉴定了 E(Pc) 的两个关键靶标。首先,E(Pc) 抑制 CycB 的转录,可能通过调节 H4 乙酰化。其次,E(Pc) 对于积累重要的生殖细胞分化因子 Bag-of-marbles (Bam) 是必需的,这是通过转录后调控实现的。当 E(Pc) 下调时,CycB 的增加和 Bam 的减少都会导致生殖细胞有丝分裂到减数分裂的转变缺陷。此外,在生理条件下和从热休克诱导的内切酶表达恢复后,生殖细胞中 E(Pc) 的失活会导致双链 DNA 断裂 (DSB) 的积累。强大的 DSB 修复的失败可能导致生殖细胞的丧失。最后,削弱组蛋白乙酰转移酶 Tip60 的活性会导致类似于 E(Pc) 功能丧失的生殖细胞缺陷,这表明 E(Pc) 与 Tip60 协同作用。总之,我们的数据表明 E(Pc) 在维持雄性生殖细胞活性和基因组完整性方面具有多效性作用。我们的发现将有助于阐明 E(Pc) 的体内分子机制。