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Bazooka/PAR3 is dispensable for polarity in Drosophila follicular epithelial cells.

Shahab J, Tiwari MD, Honemann-Capito M, Krahn MP, Wodarz A - Biol Open (2015)

Bottom Line: While all these baz alleles display identical phenotypes during embryonic epithelial development, we observe strong discrepancies in the severity and penetrance of polarity defects in the follicular epithelium: polarity is mostly normal in baz(EH747) and baz(XR11) while baz(4) and baz(815) (-8) show loss of polarity, severe multilayering and loss of epithelial integrity throughout the clones.Further analysis reveals that the chromosomes carrying the baz(4) and baz(815-8) alleles may contain additional mutations that enhance the true baz loss-of-function phenotype in the follicular epithelium.This study clearly shows that Baz is dispensable for the regulation of polarity in the follicular epithelium, and that the requirement for key regulators of cell polarity is highly dependent on developmental context and cell type.

View Article: PubMed Central - PubMed

Affiliation: Stammzellbiologie, Institut für Anatomie und Zellbiologie, Georg-August Universität Göttingen, Justus-von-Liebig-Weg 11, 37077 Göttingen, Germany.

No MeSH data available.


Related in: MedlinePlus

Localization of DE-cad and aPKC are unaffected in bazXR11 and bazEH747 FE clones.Ovarian follicles in which bazXR11 (A–A″″), bazEH747 (B–B″″), baz815-8 (C–C″″) and baz4 (D-D″″) mutant cells were induced by hs-Flp mediated recombination and marked by loss of His-GFP. White boxes in A,B,C,D indicate regions shown in A′–A″″, B′–B″″, C′–C″″ and D–D″″, respectively. Follicles were stained with DE-cad, aPKC and Dlg as indicated. Neither DE-cad nor aPKC apical localization is affected in bazXR11 (A″ and A′″) or bazEH747 (B″ and B′″) mutant cells. Many baz815-8 mutant cells show wild type localization of aPKC and DE-cad as indicated by arrows (C–C″″). Some baz815-8 mutant cells in which cell shape has been compromised appear to lose apical aPKC and junctional DE-cad staining as indicated by an arrowhead (C). Many baz4 mutant FE cells retain junctional DE-cad localization even in the absence of apical aPKC localization as indicated by arrows (D–D″″). Others show a loss of both apical aPKC and junctional DE-cad as indicated by an arrowhead (D). Scale bars = 20 µm (A–D); 5 µm (all other scale bars).
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f06: Localization of DE-cad and aPKC are unaffected in bazXR11 and bazEH747 FE clones.Ovarian follicles in which bazXR11 (A–A″″), bazEH747 (B–B″″), baz815-8 (C–C″″) and baz4 (D-D″″) mutant cells were induced by hs-Flp mediated recombination and marked by loss of His-GFP. White boxes in A,B,C,D indicate regions shown in A′–A″″, B′–B″″, C′–C″″ and D–D″″, respectively. Follicles were stained with DE-cad, aPKC and Dlg as indicated. Neither DE-cad nor aPKC apical localization is affected in bazXR11 (A″ and A′″) or bazEH747 (B″ and B′″) mutant cells. Many baz815-8 mutant cells show wild type localization of aPKC and DE-cad as indicated by arrows (C–C″″). Some baz815-8 mutant cells in which cell shape has been compromised appear to lose apical aPKC and junctional DE-cad staining as indicated by an arrowhead (C). Many baz4 mutant FE cells retain junctional DE-cad localization even in the absence of apical aPKC localization as indicated by arrows (D–D″″). Others show a loss of both apical aPKC and junctional DE-cad as indicated by an arrowhead (D). Scale bars = 20 µm (A–D); 5 µm (all other scale bars).

Mentions: We started by comparing the effects of the different alleles on the localization of aPKC and DE-cad in the lateral FE. Neither bazXR11 (Fig. 6A–A″″) nor bazEH747 (Fig. 6B–B″″) clones showed any difference in the localization of aPKC or DE-cad compared to neighboring wild type cells. Furthermore, baz GFP RNAi knockdown FE cells showed normal apical localization of aPKC and basolateral localization of Lgl (supplementary material Fig. S2C–C′″).


Bazooka/PAR3 is dispensable for polarity in Drosophila follicular epithelial cells.

Shahab J, Tiwari MD, Honemann-Capito M, Krahn MP, Wodarz A - Biol Open (2015)

Localization of DE-cad and aPKC are unaffected in bazXR11 and bazEH747 FE clones.Ovarian follicles in which bazXR11 (A–A″″), bazEH747 (B–B″″), baz815-8 (C–C″″) and baz4 (D-D″″) mutant cells were induced by hs-Flp mediated recombination and marked by loss of His-GFP. White boxes in A,B,C,D indicate regions shown in A′–A″″, B′–B″″, C′–C″″ and D–D″″, respectively. Follicles were stained with DE-cad, aPKC and Dlg as indicated. Neither DE-cad nor aPKC apical localization is affected in bazXR11 (A″ and A′″) or bazEH747 (B″ and B′″) mutant cells. Many baz815-8 mutant cells show wild type localization of aPKC and DE-cad as indicated by arrows (C–C″″). Some baz815-8 mutant cells in which cell shape has been compromised appear to lose apical aPKC and junctional DE-cad staining as indicated by an arrowhead (C). Many baz4 mutant FE cells retain junctional DE-cad localization even in the absence of apical aPKC localization as indicated by arrows (D–D″″). Others show a loss of both apical aPKC and junctional DE-cad as indicated by an arrowhead (D). Scale bars = 20 µm (A–D); 5 µm (all other scale bars).
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Related In: Results  -  Collection

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f06: Localization of DE-cad and aPKC are unaffected in bazXR11 and bazEH747 FE clones.Ovarian follicles in which bazXR11 (A–A″″), bazEH747 (B–B″″), baz815-8 (C–C″″) and baz4 (D-D″″) mutant cells were induced by hs-Flp mediated recombination and marked by loss of His-GFP. White boxes in A,B,C,D indicate regions shown in A′–A″″, B′–B″″, C′–C″″ and D–D″″, respectively. Follicles were stained with DE-cad, aPKC and Dlg as indicated. Neither DE-cad nor aPKC apical localization is affected in bazXR11 (A″ and A′″) or bazEH747 (B″ and B′″) mutant cells. Many baz815-8 mutant cells show wild type localization of aPKC and DE-cad as indicated by arrows (C–C″″). Some baz815-8 mutant cells in which cell shape has been compromised appear to lose apical aPKC and junctional DE-cad staining as indicated by an arrowhead (C). Many baz4 mutant FE cells retain junctional DE-cad localization even in the absence of apical aPKC localization as indicated by arrows (D–D″″). Others show a loss of both apical aPKC and junctional DE-cad as indicated by an arrowhead (D). Scale bars = 20 µm (A–D); 5 µm (all other scale bars).
Mentions: We started by comparing the effects of the different alleles on the localization of aPKC and DE-cad in the lateral FE. Neither bazXR11 (Fig. 6A–A″″) nor bazEH747 (Fig. 6B–B″″) clones showed any difference in the localization of aPKC or DE-cad compared to neighboring wild type cells. Furthermore, baz GFP RNAi knockdown FE cells showed normal apical localization of aPKC and basolateral localization of Lgl (supplementary material Fig. S2C–C′″).

Bottom Line: While all these baz alleles display identical phenotypes during embryonic epithelial development, we observe strong discrepancies in the severity and penetrance of polarity defects in the follicular epithelium: polarity is mostly normal in baz(EH747) and baz(XR11) while baz(4) and baz(815) (-8) show loss of polarity, severe multilayering and loss of epithelial integrity throughout the clones.Further analysis reveals that the chromosomes carrying the baz(4) and baz(815-8) alleles may contain additional mutations that enhance the true baz loss-of-function phenotype in the follicular epithelium.This study clearly shows that Baz is dispensable for the regulation of polarity in the follicular epithelium, and that the requirement for key regulators of cell polarity is highly dependent on developmental context and cell type.

View Article: PubMed Central - PubMed

Affiliation: Stammzellbiologie, Institut für Anatomie und Zellbiologie, Georg-August Universität Göttingen, Justus-von-Liebig-Weg 11, 37077 Göttingen, Germany.

No MeSH data available.


Related in: MedlinePlus