Fig. 7. Loss of tinman in larval and adult hearts severely compromises its structure and function. (A,B) F-actin (phalloidin) staining of regions of third instar larval dorsal vessels. In the wild type (A, posterior aorta; A', heart), the myofibrils are arranged in a helical network, whereas in tin-ABD, tin³⁴⁶/tin^EC40 mutant animals (B, posterior aorta; B', heart), the myofibrils run largely parallel to the AP axis and are highly irregular in the posterior heart region. (C-F) -Actinin staining of 2-day-old adult hearts at low (C,D) and high magnifications (E,F). The tin mutant hearts (arrows in D, F; tin-ABD; tin-ABD, tin³⁴⁶/tin^EC40) are much narrower because of severe hypotrophy and have less intensely -actinin-stained myofibrils than do heterozygous controls (C,E). Spiral myofibrils are lacking in the cardiac tin mutant (F). We also observe a much-reduced contractility of these hearts (data not shown). (G) Pacing-induced failure rates for flies with absent cardiac Tin (tin-ABD, tin³⁴⁶/tin³⁴⁶ and tin-ABD; tin-ABD, tin³⁴⁶/tin^EC40; 2- to 3-day-old adults) paced by external electrical stimuli to 6 Hz for 30 seconds. Failure rates are dramatically increased in flies lacking cardiac tin expression beginning at mid-embryonic stages to adulthood. (H) Recovery rate from pacing-induced heart failure is dramatically decreased in flies with absent cardiac tin function. The flies with heart failure (arrested or fibrillating) were monitored for recovery from failure to a regular heartbeat for 2 minutes after pacing (recovery rate). (I) Demographic survivorship of flies with ablated cardiac tin expression showing a much-reduced lifespan of these flies.