UASt regulatory sequences drive expression of an inverted repeat.
Adult glia expressing mbcGD6965 (through Scer\GAL4repo and Scer\GAL80ts.αTub84B) exhibit reduced recruitment of glial cells to severed axons, resulting in a delay in axonal debris clearance.
Expression of mbcGD6965 under the control of Scer\GAL4alrm.PD results in a mild suppression of mushroom body γ neuron pruning at 18 hours after pupal formation and a mild phenotype in adults.
The expression of mbcGD6965 under the control of Scer\GAL4srp.Hemo does not affect the competence of embryonic hemocytes of undertaking phagocytosis of apoptotic cells, as compared to controls.
The expression of mbcGD6965 under the control of Scer\GAL4Act5C.PI leads to near lethality.
Adults expressing mbcGD6965 under the control of Scer\GAL4elav.PLu (in the presence of Dcr-2Scer\UAS.cDa to increase the efficiency of RNAi) do not show a significant defect in avoidance of noxious temperature (46[o]C) compared to control flies.
Expression under the control of Scer\GAL4Mef2.PR results in late pupal lethality.
Expression under the control of Scer\GAL4pnr-MD237 results in extra bristles on the notum in 30-40% of the Scer\GAL4pnr-MD237 expression domain.
Expression under the control of Scer\GAL4pnr-MD237 results in an enlarged notum.
Scer\GAL4repo, Scer\GAL80ts.αTub84B, mbcGD6965 has glial cell phenotype, enhanceable by Scer\GAL4repo/SosGD1539, Scer\GAL80ts.αTub84B
Scer\GAL4repo, Scer\GAL80ts.αTub84B, mbcGD6965 has vesicle phenotype, enhanceable by Scer\GAL4repo/SosGD1539, Scer\GAL80ts.αTub84B
mbcGD6965/Scer\GAL4repo, Scer\GAL80ts.αTub84B is an enhancer of glial cell phenotype of Scer\GAL4repo, Scer\GAL80ts.αTub84B, SosGD1539
mbcGD6965/Scer\GAL4repo, Scer\GAL80ts.αTub84B is an enhancer of vesicle phenotype of Scer\GAL4repo, Scer\GAL80ts.αTub84B, SosGD1539
Adult glia expressing SosGD1539 and mbcGD6965 (through Scer\GAL4repo and Scer\GAL80ts.αTub84B) exhibit complete blockage of glial recruitment to axonal injury sites. This results in the accumulation of axonal debris and a glial hypertrophy response.