
Phenotypes of Drosophila with germline-specific shu knockdown. (A) Depletion of shu in the germline results in derepression of multiple, unrelated transposons from the LINE and LTR families. Derepression, relative to white RNAi, is displayed as log2 fold change in heat map form. Analysis of flies with germline knockdown of Armi and Piwi, two known piRNA components, is displayed for comparison. (B) Germline-knockdown of shu causes patterning defects as indicated by the presence of fused dorsal appendages. (C) Depletion of shu causes female sterility. shu RNAi females lay fewer eggs compared with controls or animals depleted of other piRNA pathway factors. Hatching rates for all knockdown animals are zero, indicating complete sterility. (D) Depletion of shu in the germline using nos-GAL4 results in Piwi delocalization from nuclei and in Aub and Ago3 delocalization from nuage. Vasa localization is not changed. Depletion of white is shown as control. (E) Tj-GAL4–driven knockdown of shu in somatic follicle cells also causes Piwi delocalization. RNAi against white is shown as control.










