Reference Report

Reference
Citation	Belgacem, Y.H., Martin, J.R. (2007). Hmgcr in the Corpus Allatum Controls Sexual Dimorphism of Locomotor Activity and Body Size via the Insulin Pathway in Drosophila. PLoS ONE 2(1): e187. (Export to RIS)
FlyBase ID	FBrf0192310
Publication Type	Research paper
PubMed ID	17264888
PubMed Abstract	The insulin signaling pathway has been implicated in several physiological and developmental processes. In mammals, it controls expression of 3-Hydroxy-3-Methylglutaryl CoA Reductase (HMGCR), a key enzyme in cholesterol biosynthesis. In insects, which can not synthesize cholesterol de novo, the HMGCR is implicated in the biosynthesis of juvenile hormone (JH). However, the link between the insulin pathway and JH has not been established. In Drosophila, mutations in the insulin receptor (InR) decrease the rate of JH synthesis. It is also known that both the insulin pathway and JH play a role in the control of sexual dimorphism in locomotor activity. In studies here, to demonstrate that the insulin pathway and HMGCR are functionally linked in Drosophila, we first show that hmgcr mutation also disrupts the sexual dimorphism. Similarly to the InR, HMGCR is expressed in the corpus allatum (ca), which is the gland where JH biosynthesis occurs. Two p[hmgcr-GAL4] lines were therefore generated where RNAi was targeted specifically against the HMGCR or the InR in the ca. We found that RNAi-HMGCR blocked HMGCR expression, while the RNAi-InR blocked both InR and HMGCR expression. Each RNAi caused disruption of sexual dimorphism and produced dwarf flies at specific rearing temperatures. These results provide evidence: (i) that HMGCR expression is controlled by the InR and (ii) that InR and HMGCR specifically in the ca, are involved in the control of body size and sexual dimorphism of locomotor activity.
DOI	10.1371/journal.pone.0000187
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Language of Publication	English
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Publication Type	Journal
Abbreviation	PLoS ONE
Title	PLoS ONE
Publication Year	2006-
ISBN/ISSN	1932-6203
Data from Reference
Alleles (14)
	Avic\GFP^Scer\UAS.cUa HLH106^{NTdel.Scer\UAS} Hmgcr⁰⁴⁶⁸⁴ Hmgcr^C14.5 Hmgcr^NIG.10367R Hmgcr^{Scer\UAS.cvDa} InR^NIG.18402R Scer\GAL4^c316 Scer\GAL4^da.G32 Scer\GAL4^elav-C155 Scer\GAL4^Hmgcr.A Scer\GAL4^Hmgcr.B Scer\GAL4^{Scer\FRT.Act5C} Scer\GAL4^to.PD
Constructs (11)
	P{AyGAL4} P{GAL4-da.G32} P{Hmgcr.A-Gal4} P{Hmgcr.B-Gal4} P{NIG.10367R} P{NIG.18402R} P{PZ} P{to-GAL4.D} P{UAS-GFP.U} P{UAS-HLH106.NTdel} P{UAS-Hmgcr.vD}
Genes (6)
	Akh Avic\GFP HLH106 Hmgcr InR Scer\GAL4
Insertions (5)
	P{GawB}c316 P{GawB}elav^C155 P{NIG.10367R}1 P{NIG.10367R}3 P{PZ}Hmgcr⁰⁴⁶⁸⁴
Natural transposons (1)
	P-element