Mobilization of P{EP}sggGE3785-9, removing 1.8kb from the 3' end of PI4KIIIα. This deletes the entire predicted kinase domain and the majority of the upstream PIK accessory domain of PI4KIIIα, and part of the first exon of sgg.
C-terminal deletion of PI4KIIIalpha removing the entire kinase domain and part of the upstream PIK domain.
No eggs are recovered upon induction of PI4KIIIαΔ123 germline clones (GLCs). In 50% of stage 9 or later egg chambers, nurse cell nuclei are found in the ooplasm rather than being restricted to the anterior of the egg chamber. Organization of the overlying layer of follicle cells also appears irregular. Mutant egg chambers at later stages show evidence of border cell migation and nurse cell dumping, but lack dorsal appendages. Late stage GLCs exhibit pycnotic nuclei and appear to degenerate.
Ring canals cluster towards the center of the cyst in early PI4KIIIαΔ123 germline clones.
In contrast to prominent membranes separating wild type nurse cell nuclei, PI4KIIIαΔ123 germline clones (GLCs) have vesiculated membranes around clustered ring canals, thin membranes between some nurse cell nuclei, and none between others; in addition, membranes terminate within the cytoplasm. In early PI4KIIIαΔ123 GLC egg chambers with more severe phenotypes, the somatic follicular epithelium that normally encapsulates the cyst also degenerates or is missing. In late stage GLCs, membranes are seen between some nuclei but not others.
cis-Golgi morphology is not grossly affected in PI4KIIIαΔ123 germline clones.
PI4KIIIαΔ123 germline clones exhibit polarity defects in the egg chamber, as evidenced by molecular markers and the fact the oocyte nucleus fails to localize at the dorsal-anterior position.
Pi4KIIIαΔ123 is rescued by Pi4KIIIα+tTa
PI4KIIIα+tTa fully rescues PI4KIIIαΔ123 mutants to viability, and rescues the ring canal phenotype seen in PI4KIIIαΔ123 germline clones.
