Histone H1-mediated epigenetic regulation controls germline stem cell self-renewal by modulating H4K16 acetylation

Jin Sun, Hui-Min Wei, Jiang Xu, Jian-Feng Chang, Zhihao Yang, Xingjie Ren, Wen-Wen Lv, Lu-Ping Liu, Li-Xia Pan, Xia Wang, Huan-Huan Qiao, Bing Zhu, Jun-Yuan Ji, Dong Yan, Ting Xie, Fang-Lin Sun () and Jian-Quan Ni ()
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Jin Sun: School of Medicine, Tsinghua University
Hui-Min Wei: Research Center for Translational Medicine at East Hospital, School of Life Sciences and Technology, Tongji University
Jiang Xu: School of Medicine, Tsinghua University
Jian-Feng Chang: Research Center for Translational Medicine at East Hospital, School of Life Sciences and Technology, Tongji University
Zhihao Yang: School of Medicine, Tsinghua University
Xingjie Ren: School of Medicine, Tsinghua University
Wen-Wen Lv: School of Medicine, Tsinghua University
Lu-Ping Liu: School of Medicine, Tsinghua University
Li-Xia Pan: School of Medicine, Tsinghua University
Xia Wang: School of Medicine, Tsinghua University
Huan-Huan Qiao: School of Medicine, Tsinghua University
Bing Zhu: Institute of Biophysics, Chinese Academy of Sciences
Jun-Yuan Ji: College of Medicine, Texas A&M Health Science Center
Dong Yan: Harvard Medical School
Ting Xie: Stowers Institute for Medical Research
Fang-Lin Sun: Research Center for Translational Medicine at East Hospital, School of Life Sciences and Technology, Tongji University
Jian-Quan Ni: School of Medicine, Tsinghua University

Nature Communications, 2015, vol. 6, issue 1, 1-10

Abstract: Abstract Epigenetics plays critical roles in controlling stem cell self-renewal and differentiation. Histone H1 is one of the most critical chromatin regulators, but its role in adult stem cell regulation remains unclear. Here we report that H1 is intrinsically required in the regulation of germline stem cells (GSCs) in the Drosophila ovary. The loss of H1 from GSCs causes their premature differentiation through activation of the key GSC differentiation factor bam. Interestingly, the acetylated H4 lysine 16 (H4K16ac) is selectively augmented in the H1-depleted GSCs. Furthermore, overexpression of mof reduces H1 association on chromatin. In contrast, the knocking down of mof significantly rescues the GSC loss phenotype. Taken together, these results suggest that H1 functions intrinsically to promote GSC self-renewal by antagonizing MOF function. Since H1 and H4K16 acetylation are highly conserved from fly to human, the findings from this study might be applicable to stem cells in other systems.

Date: 2015
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DOI: 10.1038/ncomms9856

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