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Article #8 Summary

2 Pages
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Department
Cell and Systems Biology
Course Code
CSB428H1
Professor
U.Tepass

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CSB428H1F Article #8: Siegrist et al.Drosophila MT induced Pins/Gi
Introduction
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
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Description
CSB428H1F Article #8: Siegrist et al. Drosophila MT induced PinsGi Introduction Astral MT, kinesin, Dlg induce cortical polarization of PinG i in neuroblasts. The cortical domain generates spindle asymmetry, daughter cell size asymmetry and sibling fates. Kinesin localizes to (+) ends, and Dlgkinesin, DlgPins co-immunoprecipitate, suggesting polarity is induced by Dlgkinesin interactions MTKinesinDlg pathway acts in parallel to InscuteablePar pathway, but Inscuteable pathway is at prophase coordinating with CNS and MT pathway is at metaphase coordinating mitotic spindle axis. Neuroblast cortical polarity involves BazaPKCPar-6 and Insc, Partner of Insc (Pins, G i to the apical cortex during interphase. At metaphase NMY-2, Dlg, Scrib and Lgl localize to apical as well. Astral MT induce pinsGiDlg cortical polarity at metaphase insc mutant lacks apical InscBazaPKCPar-6, but PinsGiDlg still formed crescents. The crescents were found all around cortex abnormally and delayed from prophase to metaphase. This suggests formation of PinsGiDlg crescents at metaphase is independent of InscP
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