tinEC40/tinABD mutant embryos show cardioblast (CB) patterning defects.
tinEC40/+ flies do not exhibit a significantly increased pacing-induced heart failure rate.
The myofibrils of the dorsal vessel are arranged almost exclusively in an anterior-posterior orientation in tinABD ; tin346/tinEC40 larvae, in contrast to wild-type larvae where they are arranged spirally. In the posterior heart region of the dorsal vessel the pattern of myofibrils is highly irregular in the mutant larvae, forming abnormal cross-shaped or 'knotted' patterns. The aorta appears thinner than normal in the mutant larvae, whereas the heart frequently has a wider diameter than normal.
The heart tube is much thinner than normal in tinABD ; tin346/tinEC40 adults. The mutant myofibrils are arranged longitudinally and transverse spirally arranged myofibrils are almost completely absent.
tinABD ; tinABD tin346/tinEC40 adults show a dramatic increase in heart failure rate after pacing of the heart by external electrical stimulus compared to the heart failure rate of control adults. The recovery rate after heart failure is dramatically decreased in the mutant adults.
tinABD ; tinABD tin346/tinEC40 adults have a reduced lifespan compared to controls.
In tinEC40 mutant embryos, the lymph gland and heart fail to form.
Mutant embryos have defects in the forming mesoderm around the foregut, but do form foregut ectoderm. 65% of mutant embryos have excess cells in the dorsal midline of the b1 region of the embryonic brain; the area occupied by neuronal nuclei is increased compared to wild type. The preoral brain commissure is abnormally thin. At late embryonic stage 13, mutant embryos show a reduction in the number of apoptotic cells at the dorsal midline of the brain compared to wild type. The number of brain ganglionic mother cells is unaffected in stage 11 mutant embryos.
Mutant embryos have mild defects in the development of the tracheal dorsal trunk.
The ordered files of cells seen in wild-type midgut visceral muscle primordia are not seen in these mutant embryos. The meso18E staining cells appear to invaginate, however, movement towards the interior is ragged and no ordered file of cells form.
Visceral mesoderm and cardiac progenitors do not form in mutant embryos.
Heart and visceral mesoderm and a subset of the somatic muscle founders fail to form in tin mutant embryos.
Some homozygous embryos hatch and survive as first instar larvae, even though they have midgut and body wall muscle defects. They fail to grow and show lethargic behavior and large midguts. The transverse nerve is missing, as are the dorsal neurohemal organs. Both the dorsal and ventral lateral bipolar dendrite neuron are disrupted when the transverse nerve is not formed. Segmental nerve b target muscles are abnormally innervated, and this is often associated with the loss of some muscle fibres. Transverse nerve exit glial cell cannot be found.
Only small islands of visceral mesoderm remain. Those principle midgut epithelial cells that are in contact with the islands of visceral mesoderm assume an epithelial phenotype.
Lack visceral muscles of the midgut though not the hindgut. The midgut constriction fail to form. The heart fails to develop: cardioblasts are not formed. Somatic muscle pattern is moderately affected, with the most extreme defect in the dorsal-most muscles.