High impact information on Rheb

• Rheb promotes cell growth as a component of the insulin/TOR signalling network [1].
• Increased levels of Rheb in Drosophila melanogaster promote cell growth and alter cell cycle kinetics in multiple tissues [1].
• In mitotic tissues, overexpression of Rheb accelerates passage through G1-S phase without affecting rates of cell division, whereas in endoreplicating tissues, Rheb increases DNA ploidy [1].
• Rheb is an essential regulator of S6K in controlling cell growth in Drosophila [2].
• We show that the defect in arginine uptake in cells lacking tsc2+ is rescued by the expression of a dominant negative form of rhb1+, the Rheb homolog in S. pombe, but not by expressing wild-type rhb1+ [3].

Biological context of Rheb

• Here, we show that signaling through TOR and its upstream regulators PI3K and Rheb is necessary and sufficient to suppress starvation-induced autophagy in the Drosophila fat body [4].
• Overexpression of dRheb in the developing fly (using the GAL4:UAS system) causes dramatic overgrowth of multiple tissues: in the wing, this is due to an increase in cell size; in cultured cells, dRheb overexpression results in accumulation of cells in S phase and an increase in cell size [5].
• In a screen to identify genes affecting hindgut morphogenesis in Drosophila, we identified a P-element insertion in dRheb, a novel, highly conserved member of the Ras superfamily of G-proteins [5].
• In Drosophila, we find that overexpression of Drosophila Rheb (dRheb) in S2 cells causes their accumulation in S phase and an increase in cell size [6].
• Overexpression of dRheb results in increased cell and tissue size without an increase in cell number; reduction of dRheb function results in reduced cell and tissue size [6].

Anatomical context of Rheb

• Inhibition of dRheb activity in cultured cells results in their arrest in G1 and a reduction in size [5].

References