Notch signaling controls GSC-niche adhesion via E-cadherin.

<p>(A) Mitotic recombination was used to generate GSCs lacking <i>N</i> and <i>Gal80</i> (Gal80 suppresses GAL4 expression). Females carried a wild-type (wt) allele linked to a <i>tub-GAL80</i> transgene <i>in trans</i> with an <i>N</i> mutant (mut) allele on one X chromosome, and <i>non-GAL4</i>, <i>UASp-mCD8GFP</i>, and <i>UAS-shg^RNAi</i> on the third chromosome. FLP-mediated recombination between <i>FRT</i> sites during mitotic division generated an <i>N</i> homozygous mutant cell lacking GAL80 (identifiable by the presence of GFP expression), which enabled transcription of <i>GFP</i> and <i>shg^RNAi</i> via the binding of GAL4 onto UAS elements. (B–D) One-week (w)-old mosaic germaria with GFP (green, mutant cells), 1B1 (red, GSC fusomes), and LamC (red, cap cell nuclear envelopes) labels. GFP-positive (⁺) GSCs and their daughter cells are outlined by dashed lines. Control (ctrl) germarium (B) contains one wt and one GFP⁺ GSC and their progeny, <i>N^55e11</i> mutant germarium (C) contains two GFP⁺ GSCs (full GSC clone) and their progeny, while <i>shg^RNAi</i>-knock down <i>N^55e11</i> mutant germarium (D) contain no GFP⁺ GSCs, but do contain their progeny, indicating that GFP⁺ GSCs have been lost from the niche. B′-D′ show the GFP channel only. Scale bar: 5 µm. (E) Relative percentage of GSC clones (as a proportion of total GSCs) at 1 and 2w after clone induction. The number of mosaic germaria analyzed is shown above each bar. **, <i>P</i><0.01. Error bar, mean ± SEM. The genotype of the control germaria is <i>hs-flpneoFRT19A/GAL80FRT19A</i>.