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. 2021 Jan 29;31(7):801–813. doi: 10.1038/s41422-020-00454-w

Fig. 1. Loss of cathD leads to morphological defects in actin-based sensory organs.

Fig. 1

ae Representative scanning electron microscope (SEM) images reveal morphological defects of actin-based sensory organs (indicated by arrows) in cathD1 mutant flies, including: ectopic bristles on the scutellum (a), disrupted actin organization on the bristle surface (b), aberrant split ends of antenna (c), microchaete with split tips (d), and ectopic ocellar bristles (e). Homozygous cathD1 mutants (ae) and hemizygous mutants carrying Df(2R)CA53 that deletes the entire cathD gene region on the second chromosome (e) were examined. f Representative images of notum bristles stained for F-actin (red) at 34 h after pupal formation (APF). cathD1 bristles exhibit disorganized microvillar-like short protrusions at the tips, whereas the wild-type bristles consist of organized parallel actin bundles. Lower panels, magnified views of dashed areas. g Scutellar bristles in adult flies were classified as follows based on severity: normal (gray, 4 bristles per scutellum), weak (orange, 5 bristles per scutellum), strong (green, 6 bristles per scutellum), and severe (dark red, > 6 bristles per scutellum). n = 120–423 flies per genotype from five independent experiments. cathD1 flies exhibit a significantly higher percentage of ectopic bristle number in both males and females, which could be restored by ubiquitous expression of wild-type human cathD (cathD1; da > cathDwt) or proteolytically inactive cathD (cathD1; da > cathDD231N). Scale bars, 50 μm for a, e, 10 μm for b, and 5 μm for c, d, f.