Author
Listed:
- 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
College of Bioengineering, Hubei University of Technology)
- 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
Tsinghua Fly Center, 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
University of Kansas School of Medicine)
- 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)
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.
Suggested Citation
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, 2015.
"Histone H1-mediated epigenetic regulation controls germline stem cell self-renewal by modulating H4K16 acetylation,"
Nature Communications, Nature, vol. 6(1), pages 1-10, December.
Handle:
RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9856
DOI: 10.1038/ncomms9856
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