trh1 mutant embryos do not exhibit tracheal invagination with no local apical constrictions or cell-shape changes occurring, with the epithelium remaining flat.
in trh1 mutant embryos, there is no specific accumulation of either actin or myosin at the invaginating edge.
In trh1 homozygous embryos, salivary duct cells fail to invaginate, instead remaining clustered on the surface of the embryo.
Homozygous mutant embryos have no tracheal tubules.
Mutants lack tracheal cell identity.
In homozygous embryos the Malpighian tubules empty into a single large sack that is attached to the hindgut and no ureters are evident (in contrast to wild-type embryos where the two anterior tubules join in a common ureter and the two posterior tubules join in a common ureter, so that two ureters empty into the hindgut). The sack could result from the malformation of either the proximal tubules or the ureters. The more distal segments of the tubules, although tubular, fail to elongate or undergo cell rearrangement, resulting in tubules that are less than 1/2 the length and wider than normal tubules. The hindguts are normal in shape but somewhat shorter than normal.
The filzkorper do not elongate and trachea do not form properly. The oesophagus, gastric caecae and Malpighian tubules are unaffected.
Tracheal structures are not formed in the embryo. Only small invaginations can occasionally be detected. Salivary ducts do not form and the filzkorper are defective.
Trachea absent. Majority of sensory nerves form normally, though incidence of misrouted axons is significantly increased, elongation of axons is slowed and sensory neurons which fail to send out an axon are frequent. These defects are seen most strongly in trh1, twi1 double mutants where neither trachea nor muscles are present.
embryonic lethal. Tracheae are absent and filzkorper not elongated.