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Retinoblastoma tumor suppressor protein in pancreatic progenitors controls ?- and ?-cell fate.

ABSTRACT: Pancreatic endocrine cells expand rapidly during embryogenesis by neogenesis and proliferation, but during adulthood, islet cells have a very slow turnover. Disruption of murine retinoblastoma tumor suppressor protein (Rb) in mature pancreatic ?-cells has a limited effect on cell proliferation. Here we show that deletion of Rb during embryogenesis in islet progenitors leads to an increase in the neurogenin 3-expressing precursor cell population, which persists in the postnatal period and is associated with increased ?-cell mass in adults. In contrast, Rb-deficient islet precursors, through repression of the cell fate factor aristaless related homeobox, result in decreased ?-cell mass. The opposing effect on survival of Rb-deficient ?- and ?-cells was a result of opposing effects on p53 in these cell types. As a consequence, loss of Rb in islet precursors led to a reduced ?- to ?-cell ratio, leading to improved glucose homeostasis and protection against diabetes.

SUBMITTER: Cai EP 

PROVIDER: S-EPMC3767525 | biostudies-literature | 2013 Sep

REPOSITORIES: biostudies-literature

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Retinoblastoma tumor suppressor protein in pancreatic progenitors controls α- and β-cell fate.

Cai Erica P EP   Wu Xiaohong X   Schroer Stephanie A SA   Elia Andrew J AJ   Nostro M Cristina MC   Zacksenhaus Eldad E   Woo Minna M  

Proceedings of the National Academy of Sciences of the United States of America 20130814 36

Pancreatic endocrine cells expand rapidly during embryogenesis by neogenesis and proliferation, but during adulthood, islet cells have a very slow turnover. Disruption of murine retinoblastoma tumor suppressor protein (Rb) in mature pancreatic β-cells has a limited effect on cell proliferation. Here we show that deletion of Rb during embryogenesis in islet progenitors leads to an increase in the neurogenin 3-expressing precursor cell population, which persists in the postnatal period and is asso  ...[more]

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