CSB428H1F Article #8: Siegrist et al.Drosophila MT induced Pins/Gi
Astral MT, kinesin, Dlg induce cort ical 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 cor tex dur ing 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 for med crescents. The crescents
were found all around cortex abno rmally and delayed from prophase to metaphase.
This suggests for mation of Pins/Gi/Dlg crescents at metaph ase is independent of Insc/Par pathway.
MT disrupting agent Colcemid treatment of insc mutant caused loss of Pins/Gi/Dlg crescents. Pins
were cytoplasmic, and Gi/Dlg was unifor mly cor tical.
Colcemid treatment did not affect WT embr yo because Pins/Gi/Dlg binds Insc/Par complex apically.
aPKC mutant lacking aPKC/Par-6 localization but retained Baz/Insc localization still for med
Pins/Gi/Dlg crescents in absence of MT showing Pins/Gi/Dlg pathway only require Insc and Baz.
WT cells treated with nocodazole lacked astral MT and cannot align their spindle, but Pins/Gi/Dlg
with Insc/Par complex at cor tex was normal.
insc mutant treated with nocodazole lost Pins/Gi/Dlg crescent. insc/fizz y double mutant showed
same loss of crescents, Pins was delocalised from the cortex, and Gi/Dlg was unifor mly cortical
This suggests astral MT is required for Pins/Gi/Dlg crescent for mation in absence of Insc/Par.
Dlg is necessary for MT induced Pins/Gi polarity
dlg/insc double mutants had defects in Pins/Gi cor tical polarity: Pins was cytoplasmic and Gi was