High impact information on Gbeta13F

• A deduced gene product from the Drosophila neurogenic locus, enhancer of split, shows homology to mammalian G-protein beta subunit [1].
• We have isolated Drosophila melanogaster mutants defective in an eye-specific G-protein beta-subunit (G beta e), and show here that the beta-subunit is essential for G-protein-receptor coupling in vivo [2].
• In ric-8 mutants, neither Galphai nor its associated beta-subunit Gbeta13F are localized at the plasma membrane, which leads to their degradation in the cytosol [3].
• These results indicate that an excess of Gbeta over Galpha is a strategy used in vivo for the suppression of spontaneous activity, thereby yielding a high signal to noise ratio, which is characteristic of the photoreceptor light response [4].
• This mutant fails to bind Gbeta13F to the membrane, indicating an essential role of cortical Ggamma1-Gbeta13F signaling in asymmetric divisions [5].

Biological context of Gbeta13F

• In contrast, Gbeta13F appears to regulate the asymmetric localization/stability of all apical components, and Gbeta13F loss of function exhibits phenotypes resembling those seen when both apical pathways have been compromised, suggesting that it acts upstream of the apical pathways [6].
• Targeted disruption of a fungal G-protein beta subunit gene results in increased vegetative growth but reduced virulence [7].
• The deduced amino acid sequence encoded by this gene, designated cpgb-1, was found to share 66.2, 65.9, and 66.7% amino acid identity with G beta homologues from human, Drosophila, and Dictyostelium origins, respectively, but only 39.7% identity with the Saccharomyces cerevisiae G beta homologue STE4 product [7].
• The role of G-beta in signal transduction is discussed in the light of its pronounced structural conservation [8].

Anatomical context of Gbeta13F

• Furthermore, the multiple equal cleavages of G beta mutant neuroblasts accompany neural defects; this finding suggests indispensable roles of eccentric division in assuring the stem cell properties of neuroblasts [9].
• Immunohistochemical and immunoblot analyses revealed that the amount of the G beta decreased in the rhabdomeric membranes and increased in the cytoplasm in the light, compared with that in the dark [10].

Other interactions of Gbeta13F

• Distinct roles of Galphai and Gbeta13F subunits of the heterotrimeric G protein complex in the mediation of Drosophila neuroblast asymmetric divisions [6].
• A G protein beta subunit gene (Gbe) is expressed only in the eyes of adult D. melanogaster [11].
• This was confirmed by the observation that light stimulation of PLC activity is deficient in mutants that lack the eye-specific G protein beta subunit G beta e [12].
• Homology modeling using the crystal structure of another WD repeat protein, the G-protein beta-subunit, predicts that esc protein adopts a beta-propeller structure [13].

Analytical, diagnostic and therapeutic context of Gbeta13F

• Immunocytochemical and in situ hybridization analyses further demonstrate that Gbe is expressed in the eyes but not in the brain, whereas Gbb is abundantly expressed in the brain [11].

References