期刊
DEVELOPMENTAL BIOLOGY
卷 379, 期 2, 页码 167-181出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ydbio.2013.04.015
关键词
dBre1; dSet1; H3K4 methylation; GSC self-renewal; Germ cell differentiation
资金
- National Basic Research Program of China [2012CB966903]
- National Natural Science Foundation of China [31171426, 81121001]
- Innovation Project of Shanghai Municipal Education Commission [12ZZ015]
The Drosophila ovarian germline stem cells (GSCs) constantly experience self-renewal and differentiation, ensuring the female fertility throughout life. The balance between GSC self-renewal and differentiation is exquisitely regulated by the stem cell niche, the stem cells themselves and systemic factors. Increasing evidence has shown that the GSC regulation also involves epigenetic mechanisms including chromatin remodeling and histone modification. Here, we find that dBre1, an E3 ubiquitin ligase, functions in controlling GSC self-renewal and germ cell differentiation via distinct mechanisms. Removal or knock down of dBrel function in the germline or somatic niche cell lineage leads to a gradual GSC loss and disruption of H3K4 trimethylation in the Drosophila ovary. Further studies suggest that the defective GSC maintenance is attributable to compromised BMP signaling emitted from the stem cell niche and impaired adhesion of GSCs to their niche. On the other hand, dBre1-RNAi expression in escort cells causes a loss of H3K4 trimethylation and accumulation of spectrosome-containing single germ cells in the germarium. Reducing dpp or dally levels suppresses the germ cell differentiation defects, indicating that dBrel limits BMP signaling activities for the differentiation control. Strikingly, all phenotypes observed in dBrel mutant ovaries can be mimicked by RNAi-based reduced expression of dSet1, a Drosophila H3K4 trimethylase. Moreover, genetic studies favor that dBrel interacts with dSet1 in controlling GSC maintenance and germ cell differentiation. Taken together, we identify a dBre1/dSet1 -dependent pathway for the H3K4 methylation involved in the cell fate regulation in the Drosophila ovary. (C) 2013 Elsevier Inc. All rights reserved.
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