This report describes a potential fly model of type 2 diabetes or related disorders using loss-of-function mutations of Dmel\Rheb, which is postulated to act in the Drosophila insulin pathway. Classical loss-of-function alleles, RNAi-targeting constructs, and alleles caused by insertional mutagenesis have been generated for the Rheb gene.
In human, there are two genes orthologous to Dmel\Rheb, RHEB and RHEBL1; RHEB encodes a lipid-anchored GTPase that has been shown to have a role in the insulin/TOR/S6K signaling pathway. The human gene Hsap\RHEB has been introduced into flies; heterologous rescue has not been tested.
Severe loss-of-function mutations of Dmel\Rheb are homozygous lethal in the larval or pupal stages. Flies with partial loss-of-function alleles exhibit significantly reduced body weight; some alleles exhibit higher total lipid content and impairment in retinal function. Genetic and physical interactions have been described for Dmel\Rheb; see below and in the Rheb gene report.
[updated Jan. 2017 by FlyBase; FBrf0222196]
RHEB is a member of the GTPase superfamily and encodes a lipid-anchored, cell membrane protein with five repeats of the RAS-related GTP-binding region. It has been shown to have a role in the insulin/TOR/S6K signaling pathway. [Gene Cards, RHEB; 2017.01.27]
Many to one (2 human to 1 Drosophila): the second orthologous gene in human is RHEB.
Many to one (2 human to 1 Drosophila): the second orthologous gene in human is RHEBL1.
High-scoring ortholog of human RHEB; moderate-scoring ortholog of RHEBL1 (1 Drosophila to 2 human). Dmel\Rheb shares 64% identity and 81% similarity with RHEB; it shares 55% identity and 74% similarity with RHEBL1.