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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
PubMed

Insights

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.
Keywords:
Beta cellDiabetesE2F6ProliferationTLX

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