-positive corpora cardiaca precursor cells are missing in stage 12 mutant embryos.
Mutant embryos form tracheal dorsoventral structures reminiscent of dorsal branches that elongate and undergo stalk-cell intercalation.
22% of twi1
/+ flies show defects in TDT organization but all twi1
/+ flies show a wild-type number of DLM fibers.
Invagination of the keyhole cells still occurs during proventriculus development.
The hindguts of mutant embryos are able to undergo a significant amount of elongation.
Homozygous mutants completely lack somatic musculature. The addition of twi2x.Scer\UAS
driven by Scer\GAL4twi.PB
to homozygous twi1
leads to animals in which somatic muscles form but with an aberrant pattern. Visceral muscle progenitors are missing as well as the majority of both pericardial and cardial heart cells. Instead multinucleated somatic muscles are found dorsally where the heart normally develops and around the gut.
Hindgut ectoderm fails to elongate properly (germband retraction fails), but forms and expresses wg
in restricted domains, as for wild type case, even though mesoderm is lacking.
In mutant embryos, formation of the tracheal tree is severely perturbed: there is no dorsal trunk and there is only some development of dorsal and ventral branches.
Malpighian tubules arrest early in their morphogenesis in homozygous embryos. The tubules are spherical at stages 16 and 17 (when they are elongated in wild-type embryos) and have more cells than recently evaginated tubules. The tip cells are present. The hindgut is apparently normal, although it is contorted due to the twistings of the mutant embryo.
Embryos develop a twisted phenotype.
Motor axons grow out of the CNS even though it is drastically malformed. In each hemisegment the nerves form a major dorsally projecting branch and in 39% cases a minor laterally projecting branch. The axons stay close together until the branch opens up at the dorsalmost tip, where there is some short range defasciculation. Active zones can be detected along the nerves.
The endoderm becomes internalized during gastrulation, but does not form an epithelium. Heterozygous twi1
embryos from heterozygous dl1
mothers lack various amounts of mesoderm in a temperature-dependent manner. Gaps in the visceral mesoderm are correlated with gaps in the overlying midgut epithelium.
Embryos lack mesodermal derivatives and die after about 24 hours. CNS develops but at the time of death lacks a smooth sheath of neural lamella, instead the surface is entirely pebbled in texture.
In spite of normal AMG and PMG invagination, neither anterior nor posterior midgut primordia shows any sign of extension towards each other, but remain as large mesenchymal cell masses immersed in yolk at the ends of the embryo. The cells of these primordia fail to arrange into an epithelium.
Somatic muscles 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
double mutants where neither trachea nor muscles are present.
Homozygous embryos do not form a ventral furrow. Mesectodermal domain is shifted ventrally.
Dorsalized embryos: all cuticle cells along the dorsoventral axis behave like dorsal cells of the wild type embryo. zen expression pattern refines at stage 5, dpp pattern does not refine at all, twi and sna are expressed during late stages of embryogenesis.
No changes in phenotype of tor13D
Small ventral furrows (consisting of 8-10 cells) are seen in twi1
mutant embryos. They are often quite deep and long and always run along the ventral midline. By the end of germ band extension the furrow flattens out again and forms a continuous epithelium with the ectoderm. Two deep folds form where the dorsal ectoderm and neuroectoderm meet.