Whereas wild-type larval neuroblasts during asymmetric cell division expand the apical cortex during anaphase, the Pkn06736/Df(2R)w73-1 mutant neuroblasts first expand the basal cortex which subsequently retracts and then the apical cortex is enlarged, causing a temporarily inverted asymmetric anaphase figure followed by a symmetric one and finally normal asymmetric figure. The cell curvature along the apical-basal neuroblast cortex from early anaphase to telophase is also abnormal in Pkn06736/Df(2R)w73-1 neuroblasts: While wild-type cells show a cortical ingression (negative curvature) in a basally shifted position at early anaphase stage, this ingression develops into a pronounced cleavage furrow but remain at approximately the location. In contrast, the mutant neuroblasts initiate furrowing close to the apical cortex and this ingression then shifts basally during anaphase.
Even prior to anaphase, during metaphase, the Pkn06736/Df(2R)w73-1 neuroblasts display significant cell shape deformation of the apical cortex - both positive and negative changes in curvature while in wild-type neuroblasts the curvature change very little during metaphase.
This abnormal shape dynamics is underpinned by spatiotemporal aberrations in myosin localization pattern and activity.
Egg length is significantly reduced in Pkn06736/Pkn06736 female germline clones.
During nurse cell dumping, egg chambers mutant for Pkn06736/Pkn06736 show increased nurse cell-to-oocyte membrane collapse, leading to abnormal presence of ring canals, border cells and/or nurse cell nuclei in the oocyte cytoplasm.
Females with Pkn06736/Pkn06736 germline clones show intermediate abnormal accumulation of F-actin in nurse cells of stage 10 egg chambers.
No adult homozygotes emerge. 10% of homozygous embryos show a dorsal closure phenotype. Germline clones produced mutant embryos, about 55% of which showed defects in dorsal closure. No defects in patterning or in the central and peripheral nervous systems or somatic muscles were found. When embryos from germline clone mothers are examined for cell shape, despite apparently normal leading edge cell stretching, all epidermal cells adopt an unstretched polygonal shape.
Pkn06736 has lethal phenotype, suppressible by Pkc53E::Pknhs.PB
Pkn06736 has lethal phenotype, non-suppressible by Pkn::Rokhs.PB
Pkn06736 has lethal phenotype, non-suppressible by Pak::Pknhs.PB
Pkn06736 has lethal phenotype, non-suppressible by Pak::Pkc53Ehs.PB
Pkn06736 has lethal phenotype, non-suppressible by Pkc53E::Rokhs.PB
Pkn06736 has lethal phenotype, non-suppressible by Pkn::Mmus\Rtknhs.PB
Pkn06736 has lethal phenotype, non-suppressible by Pkc53E::Mmus\Rtknhs.PB
Pkn06736/Pkn[+] is a suppressor of visible phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E
Pkn06736 has embryo | dorsal closure stage phenotype, enhanceable by Rho172R
Pkn06736 has embryonic epidermis | dorsal phenotype, enhanceable by Rho172R
Pkn06736 has embryo | dorsal closure stage phenotype, enhanceable by bsk1
Pkn06736 has embryonic epidermis | dorsal phenotype, enhanceable by bsk1
Pkn06736/Pkn[+] is a suppressor of wing phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E
Expression of Pkc53E::Pknhs.PB (using a reduced heat shock regime of 15 minutes per day) can partially rescue the lethality of Pkn06736.
Pkn06736/+ suppresses the mutant wing phenotype caused by expression of LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E (the % of wings with normal morphology at 18oC is increased from 9% to 27%).
Pkn06736 is partially rescued by PknG58A.hs
Pkn06736 is partially rescued by PknΔACC1.hs
Pkn06736 is partially rescued by PknΔACC2.hs
Pkn06736 is partially rescued by PknΔACC12.hs
Pkn06736 is not rescued by PknΔACC123.hs
A. Spradling.
Complements: l(2)0365903659. Complements: l(2)0384503845. Complements: l(2)45Bck05611a. Complements: Pknk11209. Complements: PknrG232. Complements: l(2)s1976s1976.