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Nat Commun. 2015 Jul 3;6:7693. doi: 10.1038/ncomms8693.

Genome-wide microRNA screening reveals that the evolutionary conserved miR-9a regulates body growth by targeting sNPFR1/NPYR.

Author information

1
1] Neurophysiology Research Group, Bio-Nano Research Centre, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, Yusong-gu, Daejeon 305-806, Korea [2] Department of Functional Genomics, Korea University of Science and Technology (UST), Daejeon 305-350, Korea.
2
Department of Biological Sciences, Korea Advanced Institute of Science and Technology (KAIST), Daejeon 305-701, Korea.
3
Neurophysiology Research Group, Bio-Nano Research Centre, Korea Research Institute of Bioscience and Biotechnology (KRIBB), 125 Gwahak-ro, Yusong-gu, Daejeon 305-806, Korea.
4
Department of Biological Sciences, Konkuk University, Seoul 143-701, Korea.
5
Chungnam National University Hospital, Daejeon 301-721, Korea.
6
School of Life Sciences, Gwangju Institute of Science and Technology (GIST), Gwangju 500-712, Korea.

Abstract

MicroRNAs (miRNAs) regulate many physiological processes including body growth. Insulin/IGF signalling is the primary regulator of animal body growth, but the extent to which miRNAs act in insulin-producing cells (IPCs) is unclear. Here we generate a UAS-miRNA library of Drosophila stocks and perform a genetic screen to identify miRNAs whose overexpression in the IPCs inhibits body growth in Drosophila. Through this screen, we identify miR-9a as an evolutionarily conserved regulator of insulin signalling and body growth. IPC-specific miR-9a overexpression reduces insulin signalling and body size. Of the predicted targets of miR-9a, we find that loss of miR-9a enhances the level of sNPFR1. We show via an in vitro binding assay that miR-9a binds to sNPFR1 mRNA in insect cells and to the mammalian orthologue NPY2R in rat insulinoma cells. These findings indicate that the conserved miR-9a regulates body growth by controlling sNPFR1/NPYR-mediated modulation of insulin signalling.

PMID:
26138755
PMCID:
PMC4506552
DOI:
10.1038/ncomms8693
[Indexed for MEDLINE]
Free PMC Article

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