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Nuclear receptor TLX regulates islet beta cell proliferation via E2F6
Xiaoli Shi1, Delin Ma1, Mengni Li1
1Department of Endocrinology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, 430030, PR China.
Biochemical and Biophysical Research Communications
|April 15, 2019
Summary
Nuclear receptor TLX promotes beta cell proliferation by downregulating E2F6. This study identifies TLX-E2F6 interaction as a key mechanism for expanding functional beta cell mass in diabetes.
Area of Science:
- Endocrinology
- Molecular Biology
- Cell Biology
Background:
- Type 1 and type 2 diabetes involve loss of functional beta cell mass.
- Restoring beta cell mass is a critical therapeutic goal.
- Previous work showed nuclear receptor TLX induces beta cell proliferation.
Purpose of the Study:
- To elucidate the molecular mechanism by which TLX regulates beta cell proliferation.
- To identify direct targets of TLX in beta cells.
- To investigate the role of E2F6 in TLX-mediated beta cell proliferation.
Main Methods:
- Chromatin immunoprecipitation sequencing (ChIP-Seq) to identify TLX targets genome-wide in beta cells.
- Analysis of E2F6 expression and its association with the cell cycle.
- Functional studies involving TLX and E2F6 coexpression in beta cells.
Main Results:
- ChIP-Seq identified direct TLX targets, including proliferation regulators.
- E2F6 was identified as a key TLX target downregulated by TLX.
- E2F6 expression inhibited beta cell proliferation, and its coexpression with TLX abrogated TLX's proliferative effects.
Conclusions:
- TLX regulates beta cell proliferation, at least in part, by downregulating E2F6.
- A direct interaction between TLX and E2F6 was revealed.
- These findings suggest TLX and E2F6 as potential targets for expanding functional beta cell mass.
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