FIG. 8.
dCsk; Stat92E mutant tissue shows reduced proliferation and increased apoptosis. (A to D) Phospho-histone staining (red spots) designates mitotic nuclei in developing larval eye-antennal discs. The anterior is toward the right. The dotted line marks the morphogenetic furrow. (A) FRT82B Ubi-GFP control; (B) dCskj1D8 EGUF eye discs are larger and contain somewhat higher numbers of mitoses anterior to the furrow; (C) dCskj1D8; Stat92E06346 EGUF eye discs are smaller with somewhat fewer mitotic cells anterior to the furrow; (D) a dCskj1D8; Stat92E06346 EGUF eye disc showing a region that fails to express the 22C10 neural marker (blue). Note the large field nearly devoid of mitotic cells (bracket) in dCskj1D8; Stat92E06346 tissue (D) within and anterior to a region that would normally express 22C10. (E) Analysis of mitosis anterior to the morphogenetic furrow in eye imaginal discs. The number of mitotic nuclei anterior to the furrow was quantified, and results were controlled for tissue mass (see Materials and Methods). Results are normalized to those of control EGUF tissue. Bars represent standard errors. (F to H) Photoreceptor cell differentiation and cell death were visualized with 22C10 (blue) and anti-active caspase 7 (red) antibodies. Little cell death is present in the control (F); the emerging eye field is apparent as organized photoreceptors in the posterior half of the eye disc. Note the increased size of the dCskJ1D8 disc (G); the flare in 22C10 staining is due to a fold in the optic stalk. (G) dCskJ1D8 EGUF clones often contain a region of cell death anterior to the eye field (arrow) but little within. (H) dCskJ1D8; Stat92E06346 EGUF eye discs contain, in addition, substantial cell death within the eye field (arrows). Bracket indicates a portion of the eye field devoid of developing photoreceptors. (I) Diagram depicting the function of dCsk within developing eye epithelia. dCsk inhibits growth and proliferation by inhibiting Src signaling. Src signaling acts through Btk29A, bsk (JNK), and Stat92E activity to induce tissue overgrowth and excess proliferation. Stat92E function is required for the survival of dCsk mutant tissue. Excess Src-Btk activity may activate proapoptotic pathways that are revealed when Stat92E function is reduced.