The insulin receptor is required for the development of the Drosophila peripheral nervous system.
PLoS ONE. 2013-09-12; 8(9): e71857
DOI: 10.1371/journal.pone.0071857
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1. PLoS One. 2013 Sep 12;8(9):e71857. doi: 10.1371/journal.pone.0071857. eCollection
2013.
The insulin receptor is required for the development of the Drosophila peripheral
nervous system.
Dutriaux A(1), Godart A, Brachet A, Silber J.
Author information:
(1)University Paris Diderot, Sorbonne Paris Cité, IJM, UMR 7592 CNRS, Paris,
France.
The Insulin Receptor (InR) in Drosophila presents features conserved in its
mammalian counterparts. InR is required for growth; it is expressed in the
central and embryonic nervous system and modulates the time of differentiation of
the eye photoreceptor without altering cell fate. We show that the InR is
required for the formation of the peripheral nervous system during larval
development and more particularly for the formation of sensory organ precursors
(SOPs) on the fly notum and scutellum. SOPs arise in the proneural cluster that
expresses high levels of the proneural proteins Achaete (Ac) and Scute (Sc). The
other cells will become epidermis due to lateral inhibition induced by the Notch
(N) receptor signal that prevents its neighbors from adopting a neural fate. In
addition, misexpression of the InR or of other components of the pathway (PTEN,
Akt, FOXO) induces the development of an abnormal number of macrochaetes that are
Drosophila mechanoreceptors. Our data suggest that InR regulates the neural genes
ac, sc and sens. The FOXO transcription factor which is localized in the
cytoplasm upon insulin uptake, displays strong genetic interaction with the InR
and is involved in Ac regulation. The genetic interactions between the epidermal
growth factor receptor (EGFR), Ras and InR/FOXO suggest that these proteins
cooperate to induce neural gene expression. Moreover, InR/FOXO is probably
involved in the lateral inhibition process, since genetic interactions with N are
highly significant. These results show that the InR can alter cell fate,
independently of its function in cell growth and proliferation.
DOI: 10.1371/journal.pone.0071857
PMCID: PMC3772016
PMID: 24069139 [Indexed for MEDLINE]