Expression of DCTN2-p50dsRNA.A.Scer\UAS.P\T under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 results in yolk depletion (measured by loss of yolk autofluorescence), appearance of abnormal large vesicles, delocalization of endocytic and fate determination factors (osk mRNA) from the oocyte cortex, compromised endocytic uptake and altered microtubule organization in the oocytes. On the ultrastructural level, these oocytes show significantly fewer yolk granules as well as cortical coated pits and vesicles and contain numerous endocytic intermediates (e.g. vesicles with partially condensed yolk) compared to controls.
DCTN2-p50RNAi.A.UAS.V22, Scer\GAL4VP16.mat.αTub67C has egg chamber phenotype, suppressible | partially by Rab5S43N.UAS, Scer\GAL4VP16.mat.αTub67C
DCTN2-p50RNAi.A.UAS.V22, Scer\GAL4VP16.mat.αTub67C has vesicle | female | adult stage phenotype, suppressible | partially by Rab5S43N.UAS, Scer\GAL4VP16.mat.αTub67C
The number of oocytes containing abnormal large vesicles observed upon DCTN2-p50dsRNA.A.Scer\UAS.P\T-driven expression of Scer\GAL4mat.αTub67C.T:Hsim\VP16 is significantly reduced by co-expression of Rab5S43N.Scer\UAS.
DCTN2-p50RNAi.A.UAS.V22 is partially rescued by DCTN2-p50vas.GFP/Scer\GAL4VP16.mat.αTub67C
The yolk depletion and the endocytosis defects as well as the delocalization of osk mRNA observed in egg chambers expressing DCTN2-p50dsRNA.A.Scer\UAS.P\T under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 is significantly improved by co-expression of DCTN2-p50vas.T:Avic\GFP.