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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 Crb is 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 and Baz immunostaining. 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 anti-Baz-PDZ, aPKC and Crb antibodies as indicated. Baz is clearly absent from bazXR11 (A″), bazEH747 (B″), baz815-8 (C″) and baz4 (D″) mutant cells, respectively. No effect is seen on aPKC and Crb localization at the apical membrane in bazXR11 (A′ and A′″) and bazEH747 (B′ and B′″) mutant cells. Furthermore, no bazXR11 (A) or bazEH747 (B) mutant cells lose epithelial morphology. baz4 (D′ and D′″) mutant cells show coincident loss of aPKC and Crb from the apical membrane as indicated by white arrows. However, apical aPKC and apical Crb staining is still visible in many baz815-8 (C–C″″) and baz4 (D–D″″) mutant cells as indicated by white arrowheads. Scale bars = 20 µm (in A–D); 5 µm (all other scale bars).
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f07: Localization of Crb is 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 and Baz immunostaining. 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 anti-Baz-PDZ, aPKC and Crb antibodies as indicated. Baz is clearly absent from bazXR11 (A″), bazEH747 (B″), baz815-8 (C″) and baz4 (D″) mutant cells, respectively. No effect is seen on aPKC and Crb localization at the apical membrane in bazXR11 (A′ and A′″) and bazEH747 (B′ and B′″) mutant cells. Furthermore, no bazXR11 (A) or bazEH747 (B) mutant cells lose epithelial morphology. baz4 (D′ and D′″) mutant cells show coincident loss of aPKC and Crb from the apical membrane as indicated by white arrows. However, apical aPKC and apical Crb staining is still visible in many baz815-8 (C–C″″) and baz4 (D–D″″) mutant cells as indicated by white arrowheads. Scale bars = 20 µm (in A–D); 5 µm (all other scale bars).

Mentions: We next analyzed the effects of the different baz alleles on the localization of Crb. Our analysis of bazXR11 and bazEH747 FE clones revealed that loss of Baz had no effect on the localization of Crb (Fig. 7A,B″″). On the other hand, analysis of Crb localization in baz4 and baz815-8 FE clones yielded results similar to those for aPKC localization. In accordance with previous reports, Crb apical staining was often absent in baz4 (Fig. 7D–D″″, arrows) and baz815-8 (data not shown) mutant FE clones. However, we also observed many baz815-8 and baz4 mutant cells where Crb immunostaining appeared normal (Fig. 7C–C″″, arrowheads). Furthermore, unlike aPKC and DE-cad, aPKC and Crb localization appeared to be linked as all mutant cells that maintained apical Crb also maintained apical aPKC, while all those that showed a loss of apical Crb also showed a concomitant loss of aPKC.


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 Crb is 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 and Baz immunostaining. 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 anti-Baz-PDZ, aPKC and Crb antibodies as indicated. Baz is clearly absent from bazXR11 (A″), bazEH747 (B″), baz815-8 (C″) and baz4 (D″) mutant cells, respectively. No effect is seen on aPKC and Crb localization at the apical membrane in bazXR11 (A′ and A′″) and bazEH747 (B′ and B′″) mutant cells. Furthermore, no bazXR11 (A) or bazEH747 (B) mutant cells lose epithelial morphology. baz4 (D′ and D′″) mutant cells show coincident loss of aPKC and Crb from the apical membrane as indicated by white arrows. However, apical aPKC and apical Crb staining is still visible in many baz815-8 (C–C″″) and baz4 (D–D″″) mutant cells as indicated by white arrowheads. Scale bars = 20 µm (in A–D); 5 µm (all other scale bars).
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4400595&req=5

f07: Localization of Crb is 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 and Baz immunostaining. 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 anti-Baz-PDZ, aPKC and Crb antibodies as indicated. Baz is clearly absent from bazXR11 (A″), bazEH747 (B″), baz815-8 (C″) and baz4 (D″) mutant cells, respectively. No effect is seen on aPKC and Crb localization at the apical membrane in bazXR11 (A′ and A′″) and bazEH747 (B′ and B′″) mutant cells. Furthermore, no bazXR11 (A) or bazEH747 (B) mutant cells lose epithelial morphology. baz4 (D′ and D′″) mutant cells show coincident loss of aPKC and Crb from the apical membrane as indicated by white arrows. However, apical aPKC and apical Crb staining is still visible in many baz815-8 (C–C″″) and baz4 (D–D″″) mutant cells as indicated by white arrowheads. Scale bars = 20 µm (in A–D); 5 µm (all other scale bars).
Mentions: We next analyzed the effects of the different baz alleles on the localization of Crb. Our analysis of bazXR11 and bazEH747 FE clones revealed that loss of Baz had no effect on the localization of Crb (Fig. 7A,B″″). On the other hand, analysis of Crb localization in baz4 and baz815-8 FE clones yielded results similar to those for aPKC localization. In accordance with previous reports, Crb apical staining was often absent in baz4 (Fig. 7D–D″″, arrows) and baz815-8 (data not shown) mutant FE clones. However, we also observed many baz815-8 and baz4 mutant cells where Crb immunostaining appeared normal (Fig. 7C–C″″, arrowheads). Furthermore, unlike aPKC and DE-cad, aPKC and Crb localization appeared to be linked as all mutant cells that maintained apical Crb also maintained apical aPKC, while all those that showed a loss of apical Crb also showed a concomitant loss of aPKC.

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