Limits...
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

FE defects in bazEH747 mosaic ovaries are enhanced by loss of one copy of crb or aPKC.FE clones for FRT19A (A), bazEH747 (B), baz4 (C), bazEH747; crb11A22/+ (D), marked by absence of Ubi-GFP, were generated using the directed mosaic system by expressing UAS-Flp under the control of e22c-gal4. Lateral FE cells mutant for bazEH747 (B) look identical to FRT19A (A) control epithelia and form a continuous epithelium over the underlying nurse cells. However, mild multilayering of the FE is visible at the posterior pole of bazEH747 mosaic follicles (B, white arrowhead) as opposed to FRT19A control mosaic follicles (A). The bazEH747 mutant phenotype is strongly enhanced in a crb11A22 heterozygous mutant background (D) and appears identical to the baz4 (C) FE mutant phenotype with discontinuities in the lateral FE (white arrows) and strong multilayering at the posterior poles (white arrowheads). (E) Bar graph presenting quantitative analysis of the FEH phenotype from the baz interaction screen. All clones analyzed are hemizygous mutant for bazEH747 and heterozygous for the respective second mutation. The number of mosaic follicles with FEHs were counted and presented as an average percentage from 3 repetitions of n = 50 for each genotype listed (1% of FRT19A, 5% of bazEH747, 50% of bazEH747;aPKCK06403/+, 83% of bazEH747;crb11A22/+, 9% of bazEH747;lgl4/+, 7% of bazEH747;scrib2/+, 9% of bazEH747;par1W3/+, 10% of bazEH747;pp2aGE16781/+, 8% of bazEH747;ptenDJ189/+, 9% of bazEH747; shgR69B/+, 7% of bazEH747;ed1x5/+). At p<0.001, genotypes with same number of stars are not significantly different while those with different number of stars are significantly different. Error bars represent s.d. Scale bars = 20 µm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4400595&req=5

f05: FE defects in bazEH747 mosaic ovaries are enhanced by loss of one copy of crb or aPKC.FE clones for FRT19A (A), bazEH747 (B), baz4 (C), bazEH747; crb11A22/+ (D), marked by absence of Ubi-GFP, were generated using the directed mosaic system by expressing UAS-Flp under the control of e22c-gal4. Lateral FE cells mutant for bazEH747 (B) look identical to FRT19A (A) control epithelia and form a continuous epithelium over the underlying nurse cells. However, mild multilayering of the FE is visible at the posterior pole of bazEH747 mosaic follicles (B, white arrowhead) as opposed to FRT19A control mosaic follicles (A). The bazEH747 mutant phenotype is strongly enhanced in a crb11A22 heterozygous mutant background (D) and appears identical to the baz4 (C) FE mutant phenotype with discontinuities in the lateral FE (white arrows) and strong multilayering at the posterior poles (white arrowheads). (E) Bar graph presenting quantitative analysis of the FEH phenotype from the baz interaction screen. All clones analyzed are hemizygous mutant for bazEH747 and heterozygous for the respective second mutation. The number of mosaic follicles with FEHs were counted and presented as an average percentage from 3 repetitions of n = 50 for each genotype listed (1% of FRT19A, 5% of bazEH747, 50% of bazEH747;aPKCK06403/+, 83% of bazEH747;crb11A22/+, 9% of bazEH747;lgl4/+, 7% of bazEH747;scrib2/+, 9% of bazEH747;par1W3/+, 10% of bazEH747;pp2aGE16781/+, 8% of bazEH747;ptenDJ189/+, 9% of bazEH747; shgR69B/+, 7% of bazEH747;ed1x5/+). At p<0.001, genotypes with same number of stars are not significantly different while those with different number of stars are significantly different. Error bars represent s.d. Scale bars = 20 µm.

Mentions: We thus conducted a small-scale genetic interaction screen to test whether removing one copy of genes known to function in cell polarity enhances the bazEH747 FEH and PFC multilayering phenotypes. Quantitative analysis of the results of this screen revealed a stark increase in the penetrance of the FEH phenotype and severity of PFC multilayering in bazEH747 clones that are simultaneously heterozygous for crb11A22 or aPKCk06403 (Fig. 5). Post-hoc multiple comparison tests showed that differences in the penetrance of the FEH phenotype were significant between bazEH747; crb11A22 and all other genotypes, and bazEH747; aPKCk06403 and all other genotypes (Fig. 5). Intriguingly, bazEH747 mosaic follicles heterozygous for crb11A22 or aPKCk06403 (data not shown) were phenotypically indistinguishable from baz4 mosaic follicles (Fig. 5). These results raise the possibility that the chromosomes carrying the baz4 and baz815-8 alleles may carry second site mutations that synergistically enhance the baz loss-of-function phenotype.


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)

FE defects in bazEH747 mosaic ovaries are enhanced by loss of one copy of crb or aPKC.FE clones for FRT19A (A), bazEH747 (B), baz4 (C), bazEH747; crb11A22/+ (D), marked by absence of Ubi-GFP, were generated using the directed mosaic system by expressing UAS-Flp under the control of e22c-gal4. Lateral FE cells mutant for bazEH747 (B) look identical to FRT19A (A) control epithelia and form a continuous epithelium over the underlying nurse cells. However, mild multilayering of the FE is visible at the posterior pole of bazEH747 mosaic follicles (B, white arrowhead) as opposed to FRT19A control mosaic follicles (A). The bazEH747 mutant phenotype is strongly enhanced in a crb11A22 heterozygous mutant background (D) and appears identical to the baz4 (C) FE mutant phenotype with discontinuities in the lateral FE (white arrows) and strong multilayering at the posterior poles (white arrowheads). (E) Bar graph presenting quantitative analysis of the FEH phenotype from the baz interaction screen. All clones analyzed are hemizygous mutant for bazEH747 and heterozygous for the respective second mutation. The number of mosaic follicles with FEHs were counted and presented as an average percentage from 3 repetitions of n = 50 for each genotype listed (1% of FRT19A, 5% of bazEH747, 50% of bazEH747;aPKCK06403/+, 83% of bazEH747;crb11A22/+, 9% of bazEH747;lgl4/+, 7% of bazEH747;scrib2/+, 9% of bazEH747;par1W3/+, 10% of bazEH747;pp2aGE16781/+, 8% of bazEH747;ptenDJ189/+, 9% of bazEH747; shgR69B/+, 7% of bazEH747;ed1x5/+). At p<0.001, genotypes with same number of stars are not significantly different while those with different number of stars are significantly different. Error bars represent s.d. Scale bars = 20 µm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4400595&req=5

f05: FE defects in bazEH747 mosaic ovaries are enhanced by loss of one copy of crb or aPKC.FE clones for FRT19A (A), bazEH747 (B), baz4 (C), bazEH747; crb11A22/+ (D), marked by absence of Ubi-GFP, were generated using the directed mosaic system by expressing UAS-Flp under the control of e22c-gal4. Lateral FE cells mutant for bazEH747 (B) look identical to FRT19A (A) control epithelia and form a continuous epithelium over the underlying nurse cells. However, mild multilayering of the FE is visible at the posterior pole of bazEH747 mosaic follicles (B, white arrowhead) as opposed to FRT19A control mosaic follicles (A). The bazEH747 mutant phenotype is strongly enhanced in a crb11A22 heterozygous mutant background (D) and appears identical to the baz4 (C) FE mutant phenotype with discontinuities in the lateral FE (white arrows) and strong multilayering at the posterior poles (white arrowheads). (E) Bar graph presenting quantitative analysis of the FEH phenotype from the baz interaction screen. All clones analyzed are hemizygous mutant for bazEH747 and heterozygous for the respective second mutation. The number of mosaic follicles with FEHs were counted and presented as an average percentage from 3 repetitions of n = 50 for each genotype listed (1% of FRT19A, 5% of bazEH747, 50% of bazEH747;aPKCK06403/+, 83% of bazEH747;crb11A22/+, 9% of bazEH747;lgl4/+, 7% of bazEH747;scrib2/+, 9% of bazEH747;par1W3/+, 10% of bazEH747;pp2aGE16781/+, 8% of bazEH747;ptenDJ189/+, 9% of bazEH747; shgR69B/+, 7% of bazEH747;ed1x5/+). At p<0.001, genotypes with same number of stars are not significantly different while those with different number of stars are significantly different. Error bars represent s.d. Scale bars = 20 µm.
Mentions: We thus conducted a small-scale genetic interaction screen to test whether removing one copy of genes known to function in cell polarity enhances the bazEH747 FEH and PFC multilayering phenotypes. Quantitative analysis of the results of this screen revealed a stark increase in the penetrance of the FEH phenotype and severity of PFC multilayering in bazEH747 clones that are simultaneously heterozygous for crb11A22 or aPKCk06403 (Fig. 5). Post-hoc multiple comparison tests showed that differences in the penetrance of the FEH phenotype were significant between bazEH747; crb11A22 and all other genotypes, and bazEH747; aPKCk06403 and all other genotypes (Fig. 5). Intriguingly, bazEH747 mosaic follicles heterozygous for crb11A22 or aPKCk06403 (data not shown) were phenotypically indistinguishable from baz4 mosaic follicles (Fig. 5). These results raise the possibility that the chromosomes carrying the baz4 and baz815-8 alleles may carry second site mutations that synergistically enhance the baz loss-of-function phenotype.

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