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Fig. 5. Tin and Doc function as mutual repressors within cardioblasts. Stage 15-16 embryos carrying the svp-lacZ enhancer trap insertion AE127 heterozygously (except for C, where it is homozygous) stained for ß-galactosidase (svp-LacZ), Doc2+3 and Tin as indicated. (A) In the control, svp-LacZ and Doc2+3 are co-expressed in the Tin-negative cells (yellow arrows). rg: ring gland. (B) In a tin³⁴⁶ mutant embryo carrying tin-ABD, Doc but not svp-LacZ expression expands into all cardioblasts. (C) In a tin³⁴⁶, svp^AE127 double mutant embryo carrying tin-ABD, expression of Doc is still expanded but svp-LacZ (yellow arrows) is not. (D,E) Expanded cardiac expression of tin via S59-Mef2-HtD-Gal4 leads to Doc repression in many Svp cardioblasts (turquoise and blue arrows in D and E, respectively). Only cardioblasts lacking Tin because of variable driver activity retain Doc (E shows the embryo from D without the green channel). (F) Analogous ectopic svp1 expression causes a reduction of Tin in cardioblasts along with expansion of Doc (yellow and red arrows) and ectopic svp-lacZ in some of those cardioblasts (yellow arrows). pc, Tin⁺ pericardial cells. (G) Misexpression of Doc2 in the dorsal vessel reduces or abolishes tin expression (blue arrows), particularly in posterior cardioblasts. (H) Df(3L)DocA/Df(3L)29A6 embryo, in which levels of Doc2 and Doc3 are reduced and Doc1 is absent, show svp-lacZ and tin co-expression in numerous cardioblasts (turquoise arrows).

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