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. 2015 Oct 28;112(45):13928–13933. doi: 10.1073/pnas.1509856112

Fig. 2.

Fig. 2.

Loss of lili mutant GSCs is not caused by cell death or cell competition. (A and B) Germaria containing either WT control (A) or lili mutant (B) clonal GSCs (β-gal negative; dashed lines) do not show any activated Caspase-3 staining (red) (A′ and B′). Positive cell death control (anti-activated Caspase-3 Ab; red) stage 7–8 egg chambers are shown in Insets (Fig. S4). Clone tissue is marked by absence of β-gal (green). (C) GSCs are lost over time in hs-Gal4/UASt-liliA; lili2/lili3 females. (D) Example of a “GSC-depleted” germarium (dashed outline) stained for the germ line (Vasa; green) and membranes/spectrosomes/fusomes (1B1; red) from a 10-d-old hs-Gal4/UASt-liliA; lili2/lili3 female. (E) A similarly depleted germarium (dashed outline) attached to a lili2 mutant clonal egg chamber (β-gal present in the soma but not the germ line) stained for the spectrosome, fusome, and cell membranes marker combination Lamin C/1B1 (red). (F) Example of a GSC-depleted germarium showing developing lili2 clonal cysts (dashed outline; β-gal absent) at the site normally occupied by GSCs, staining is with anti-LamC/anti-1B1 combination (red; branched fusome is clearly visible in clonal cyst). (Scale bars: 10 μm.)