Expression of G-iα65A^{Q205L.Scer\UAS} under the control of Scer\GAL4^Bx-MS1096 induces an asymmetric cell division phenotype, resulting in stout bristle defects.

Expression of G-iα65A^Scer\UAS.cLa in glia of embryos, driven by Scer\GAL4^repo, causes defects in the formation of the blood-brain barrier, as assessed by the penetrance of a fluorescent dye into the nerve cord. The normal complement of surface glia is found at the surface of the nerve cord in G-iα65A^Scer\UAS.cLa mutants, but they are irregular in size and shape and the positioning of the nuclei is more variable than in wild type. The cortical cytoskeleton is disrupted at the cell cortex.

G-iα65A^Scer\UAS.cLa when driven by Scer\GAL4^elav.PLu has no impact on neuromuscular junction formation or viability.

74% of mitotic spindles are misoriented in the neuroblasts of embryos expressing G-iα65A^Scer\UAS.cLa under the control of Scer\GAL4^{mat.αTub67C.T:Hsim\VP16}. 80% of the neuroblasts produce two equal sized daughter cells. Expression of G-iα65A^Scer\UAS.cLa under the control of Scer\GAL4^sca-109-68 results in defects in spindle orientation in the sensory organ precursor cells.

When expression of G-iα65A^Scer\UAS.cLa is driven in the dopamine and serotonin neurons by Scer\GAL4^Ddc.PL, flies to an initial dose of cocaine compared to wild-type. Also no sensitization was seen on repeated exposures to cocaine, in contrast to wild-type. Flies expressing G-iα65A^Scer\UAS.cLa under the control of Scer\GAL4^Ddc.PL show significantly increased locomotor responses to the dopamine D2-like agonist quinpirole compared to controls. Flies expressing G-iα65A^Scer\UAS.cLa under the control of Scer\GAL4^Ddc.PL exhibit no overt behavioural or lethality phenotypes are seen.

Gαi^UAS.cLa/Scer\GAL4^elav.PLu is a non-suppressor of bouton phenotype of Gαs^B19

Gαi^UAS.cLa/Scer\GAL4^elav.PLu is a non-suppressor of synapse phenotype of Gαs^B19