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A Modifier Screen for Bazooka/PAR-3 Interacting Genes in the Drosophila Embryo Epithelium

Figure 4

Assessing early AJ phenotypes of enhanced baz zygotic mutants.

(A) Experimental set-up to analyze the DE-cad distribution of enhanced baz zygotic mutants in the F2 generation. (B) The percentage of F2 embryos displaying AJ defects detected by DE-cad staining. (C) The different types of amnioserosa AJ defects observed with DE-cad staining. The amnioserosa is bracketed. Lateral views of the embryonic body region are shown (dorsal is up and anterior is left). Normal, mild, moderate and severe defects are color-coded. Yellow arrow show abnormal clumps of DE-cad staining. DE-cad staining is lost from cell contacts in the moderate and severe categories. (D) The different types of germband AJ defects observed with DE-cad staining. The ventral neurectoderm region of the germband is bracketed. Dorsal views are shown with the anterior to the left (the germband is extended over the dorsal surface of the embryo at this stage). Normal, mild, moderate and severe defects are color-coded. Yellow arrows show groups of ventral cells that have lost DE-cad staining at cell contacts. DE-cad staining is lost from cell contacts of larger groups of cells in the moderate and severe categories. White arrowheads mark the ventral midline in each. The normal example is a lateral view showing one half of the epidermis from its most ventral edge (at the ventral mid-line) to its most dorsal edge (at the amnioserosa). The mild, moderate and severe examples focus on the ventral epidermis where the defects were seen. (E) The distribution of amnioserosa (a.s.) and germband (g.b.) AJ defects for each baz mutant enhancement identified. 4 groups are distinguished: (1) crosses which produced AJ defects in <10% of the F2 embryos (see panel B), (2) crosses which produced AJ defects in >10% of the F2 embryos (see panel B) in which <40% of amnioserosa defects were moderate or severe and >25% of germband defects were moderate or severe, (3) crosses which produced AJ defects in >10% of the F2 embryos (see panel B) in which >40% of amnioserosa defects were moderate or severe and >25% of germband defects were moderate or severe, and (4) crosses which produced AJ defects in >10% of the F2 embryos (see panel B) in which >40% of amnioserosa defects were moderate or severe and <25% of germband defects were moderate or severe. In each group the results are arranged in order of severity in the amnioserosa.

Figure 4

doi: https://doi.org/10.1371/journal.pone.0009938.g004