Central Dicer-miR-103/107 controls developmental switch of POMC progenitors into NPY neurons and impacts glucose homeostasis.

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State: Public
Version: Final published version
Serval ID
serval:BIB_CCD5949E57BA
Type
Article: article from journal or magazin.
Collection
Publications
Title
Central Dicer-miR-103/107 controls developmental switch of POMC progenitors into NPY neurons and impacts glucose homeostasis.
Journal
eLife
Author(s)
Croizier S., Park S., Maillard J., Bouret S.G.
ISSN
2050-084X (Electronic)
ISSN-L
2050-084X
Publication state
Published
Issued date
12/10/2018
Peer-reviewed
Oui
Volume
7
Language
english
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural
Publication Status: epublish
Abstract
Proopiomelanocortin (POMC) neurons are major negative regulators of energy balance. A distinct developmental property of POMC neurons is that they can adopt an orexigenic neuropeptide Y (NPY) phenotype. However, the mechanisms underlying the differentiation of <i>Pomc</i> progenitors remain unknown. Here, we show that the loss of the microRNA (miRNA)-processing enzyme <i>Dicer</i> in POMC neurons causes metabolic defects, an age-dependent decline in the number of <i>Pomc</i> mRNA-expressing cells, and an increased proportion of <i>Pomc</i> progenitors acquiring a NPY phenotype. miRNome microarray screening further identified miR-103/107 as candidates that may be involved in the maturation of <i>Pomc</i> progenitors. In vitro inhibition of miR-103/107 causes a reduction in the number of <i>Pomc</i> -expressing cells and increases the proportion of <i>Pomc</i> progenitors differentiating into NPY neurons. Moreover, in utero silencing of miR-103/107 causes perturbations in glucose homeostasis. Together, these data suggest a role for prenatal miR-103/107 in the maturation of <i>Pomc</i> progenitors and glucose homeostasis.
Keywords
Proopiomelanocortin, development, glucose homeostasis, hypothalamus, miRNA, mouse, neuroscience, obesity
Pubmed
Web of science
Open Access
Yes
Create date
08/11/2018 16:37
Last modification date
20/08/2019 15:47
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