This report describes a potential fly model of insulin pathway disorders using mutations of Dmel\tobi. tobi is postulated to act as a target of both insulin-signaling and glucagon-like signaling systems in Drosophila. UAS-overexpression and RNAi-targeting constructs have been generated for the tobi gene.
In human, there is a single high-scoring ortholog of Dmel\tobi, MYORG. MYORG is a putative glycosidase thought to act via regulation of IGF2 (insulin-like growth factor 2) activity and subsequent activation AKT (PI3K/AKT/mTOR ) signaling to promote myogenesis. The human MYORG gene has not been introduced into flies.
Flies with reduced tobi levels are viable, whereas tobi overexpression causes severe growth defects and a decrease in body glycogen; tobi expression is increased by dietary protein and decreased by dietary sugar. Physical interactions have been described for Dmel\tobi; see below and in the tobi gene report.
[updated Sep. 2018 by FlyBase; FBrf0222196]
MYORG (Myogenesis Regulating Glycosidase) is a putative glycosidase that promotes myogenesis by activating AKT signaling through the maturation and secretion of IGF2. [Gene Cards, MYORG; 2018.09.17]
One to one: 1 human to 1 Drosophila.
High-scoring ortholog of human MYORG (1 Drosophila to 1 human). Dmel\tobi shares 32% identity and 48% similarity with the human gene.
