CSB428H1 : Article #8 Summary
Document Summary
Astral mt, kinesin, dlg induce cortical polarization of pins/gi in neuroblasts. The cortical domain generates spindle asymmetry, daughter cell size asymmetry and sibling fates. kinesin localizes to (+) ends, and dlg/kinesin, dlg/pins co-immunoprecipitate, suggesting polarity is induced by dlg/kinesin interactions. mt/kinesin/dlg pathway acts in parallel to inscuteable/par pathway, but inscuteable pathway is at prophase coordinating with cns and mt pathway is at metaphase coordinating mitotic spindle axis. neuroblast cortical polarity involves baz/apkc/par-6 and insc, partner of insc (pins), gi to the apical cortex during interphase. at metaphase nmy-2, dlg, scrib and lgl localize to apical as well. Astral mt induce pins/gi/dlg cortical polarity at metaphase insc mutant lacks apical insc/baz/apkc/par-6, but pins/gi/dlg still formed crescents. The crescents were found all around cortex abnormally and delayed from prophase to metaphase. This suggests formation of pins/gi/dlg crescents at metaphase is independent of insc/par pathway. mt disrupting agent colcemid treatment of insc mutant caused loss of pins/gi/dlg crescents.