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Article #7 Summary

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

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CSB428H1F Article #7: Atwood et al. Cdc42 is downstream of Bazooka
Introduction
Cdc42 colocalize with Par-6-aPKC at the apical cor tex in a Baz dependent manner. Loss of Cdc42
or Cdc42-DN disrupts polarity and has cytoplasmic Par-6-aPKC but Baz was normal. Cdc42-CA
cause ectopic Par-6-aPKC localization.
Cdc42 increase aPKC activity by relieving Par-6 inhibition and is downstream of Baz.
Neuroblast divides unequally to produce large stem cell and small basal ganglion mother cell.
Par-6/aPKC is recruited to apical to direct Mira/Pros/Brat/Numb to basal cor tex by repressing Lgl.
In
par-6
or
aPKC
mutants. Baz is normal but basal proteins become apical.
Activated Cdc42-GTP binds to CRIB domain of Par-6.
cdc42
cant anchor Par-6-aPKC to apical cortex, same with Cdc42- DN or mutated CRIB-Par-6.
Cdc42 localize to apical cortex
Cdc42-myc in cdc42 backg round and colocalize to apical cor tex with Par-6-aPKC.
Cdc42 is downstream of Baz
Cdc42-DN expressed using
wor niu-gal4
caused Par-6 and aPKC expansion into basal cor tical
domain and expansion of Mira into apical cortical domain, suggesting aPKC is not fully active.
Baz localization was normal and cell division was normal.
Cdc42-CA produced uniform cor tical Par-6-aPKC with cytoplasmic staining and Mira into the
cytoplasm, showing Cdc42 recruited active Par-6-aPKC to entire cortex.
Baz localization was normal but cell division was symmetric.
cdc42
mutant showed cytoplasmic Par-6-aPKC and unifor mly cortical Mira but Baz was normal.
In
baz
mutant, Cdc42-myc was weakly cor tical with no apical enrichment and some cytoplasmic
staining, aPKC was cytoplasmic and Mira was unifor mly cortical.
Cdc2 is downstream of Baz to promote apical localization of Par-6-aPKC.
Cdc42 interaction with Par-6 is necessary
CRIB-PDZ of Par-6 binds Cdc42
in vitro
. Par-6
ISAA
eliminated binding.
1
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Description
CSB428H1F Article #7: Atwood et al. Cdc42 is downstream of Bazooka Introduction Cdc42 colocalize with Par-6-aPKC at the apical cortex in a Baz dependent manner. Loss of Cdc42 or Cdc42-DN disrupts polarity and has cytoplasmic Par-6-aPKC but Baz was normal. Cdc42-CA cause ectopic Par-6-aPKC localization. Cdc42 increase aPKC activity by relieving Par-6 inhibition and is downstream of Baz. Neuroblast divides unequally to produce large stem cell and small basal ganglion mother cell. Par-6aPKC is recruited to apical to direct MiraProsBratNumb to basal cortex by repressing Lgl. In par-6or aPKC mutants. Baz is normal but basal proteins become apical. Activated Cdc42-GTP binds to CRIB domain of Par-6. cdc42 cant anchor Par-6-aPKC to apical cortex, same with Cdc42-DN or mutated CRIB-Par-6. Cdc42 localize to apical cortex Cdc42-myc in cdc42 background and colocalize to apical cortex with Par-6-aPKC. Cdc42 is downstream of Baz Cdc42-DN expressed using worniu-gal4 caused Par-6 a
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