Results: 5

1.
Figure 2

Figure 2. From: Identification of genetic modifiers of CagA-induced epithelial disruption in Drosophila.

(A–F) Representative ESEM images for each class of disruption by CagA. The scoring rubric is described in Materials and Methods. (G) The mean ESEM-based eye disruption for CagA, known interactors and Moc genes of different functional classes. Error bars represent standard error.

David W. Reid, et al. Front Cell Infect Microbiol. 2012;2:24.
2.
Figure 5

Figure 5. From: Identification of genetic modifiers of CagA-induced epithelial disruption in Drosophila.

(A) Interactions of several epithelial polarity determinants with CagA, using the Dlg distribution assay described in Figure 3. Error bars represent standard error. Green asterisks represent mutants that significantly suppress CagA-induced epithelial disruption; red asterisks represent mutants that significantly enhance epithelial disruption (p < 0.05). (B) Model for the interactions of CagA with epithelial polarity determinants Cora and Crb.

David W. Reid, et al. Front Cell Infect Microbiol. 2012;2:24.
3.
Figure 3

Figure 3. From: Identification of genetic modifiers of CagA-induced epithelial disruption in Drosophila.

(A) Pattern of Dlg staining in Z-stacks of larval retinal imaginal discs. CagA-expressing eye discs are compared to those expressing the GMR-Gal4 driver alone. Shaded areas represent standard error. The arrow indicates the point at 4.8 microns below the peak intensity where the distribution was evaluated. (B) Quantification of larval retinal epithelial morphology for par1 and cora mutants, and their interactions with CagA.

David W. Reid, et al. Front Cell Infect Microbiol. 2012;2:24.
4.
Figure 1

Figure 1. From: Identification of genetic modifiers of CagA-induced epithelial disruption in Drosophila.

(A) Crossing scheme for the Moc deficiency screen. Flies containing the genetic deficiency were compared to those containing a visual marker such as CyO. Flies expressing CagA in a wild-type, (B) or egfr−/+ background, (C) were imaged by ESEM. (D) Chromosomal map of the genetic deficiency screen. The result from each deficiency (darker colors) is indicated along with the inferred functionality of each genetic region (lighter colors), where deficiencies that caused no change override those that cause enhancement or suppression.

David W. Reid, et al. Front Cell Infect Microbiol. 2012;2:24.
5.
Figure 4

Figure 4. From: Identification of genetic modifiers of CagA-induced epithelial disruption in Drosophila.

cora reduction suppresses CagA-induced epithelial disorganization but not CagA protein localization to septate junctions. (A–C) Model for the basal displacement of Dlg. Panel A represents the wild-type distribution of Dlg (represented as red structures on the lateral membranes of the epithelial cells). Panel B represents basally expanded Dlg expression due to expansion within individual cells. Panel C shows how epithelial disruption can cause basal mispositioning of Dlg expression by positioning cells deeper within the epithelium. (D) Control larval retinal epithelium (GMR-Gal4) stained with Dlg (red) and E-cad (green). YZ and XZ orthogonal planes are shown on the side and top, respectively, in D and E. Scale bar is 30 microns for all panels. (E) CagA-expressing larval retinal epithelium (GMR-Gal4; UAS-CagA) also stained with Dlg (red) and E-cad (green). Arrowhead in the upper orthogonal section shows basally mispositioned Dlg staining. Arrow indicates Dlg staining that is deep within the epithelium due to irregularities in the epithelial sheet. (F) cora+/− larval retinal epithelium expressing CagA (GMR-Gal4; UAS-CagA) showing CagA localization as labeled with anti-HA. Apical HA puncta are present. (G) A larval retinal disc expressing CagA (GMR-Gal4; UAS-CagA) labeled with HA antibody.

David W. Reid, et al. Front Cell Infect Microbiol. 2012;2:24.

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