Going Rogue: Mechanisms, Regulation, and Roles of Mutationally Activated G in Human Cancer.

G protein-coupled receptors (GPCRs) couple to heterotrimeric G proteins, comprised of and γ subunits, to convert extracellular signals into activation of intracellular signaling pathways. Canonically, GPCR-mediated activation results in the exchange of GDP for GTP on G protein subunits (G) and the dissociation of G-GTP and G protein subunits (G), both of which can regulate a variety of signaling pathways. Hydrolysis of bound GTP by G returns the protein to G-GDP and allows reassociation with G to reform the inactive heterotrimer.

Enhanced membrane binding of oncogenic G protein αqQ209L confers resistance to inhibitor YM-254890.

Heterotrimeric G proteins couple activated G protein-coupled receptors (GPCRs) to intracellular signaling pathways. They can also function independently of GPCR activation upon acquiring mutations that prevent GTPase activity and result in constitutive signaling, as occurs with the αqQ209L mutation in uveal melanoma. YM-254890 (YM) can inhibit signaling by both GPCR-activated WT αq and GPCR-independent αqQ209L.

Developing elite Neurospora crassa strains for cellulosic ethanol production using fungal breeding.

The demand for renewable and sustainable energy has generated considerable interest in the conversion of cellulosic biomass into liquid fuels such as ethanol using a filamentous fungus. While attempts have been made to study cellulose metabolism through the use of knock-out mutants, there have been no systematic effort to characterize natural variation for cellulose metabolism in ecotypes adapted to different habitats. Here, we characterized natural variation in saccharification of cellulose and fermentation in 73 ecotypes and 89 laboratory strains of the model fungus Neurospora crassa.