Overexpression of rhohs.PSt
leads to vein hypertrophy but not an increased wing area or cell division.
When heat shock drives expression of rhohs.PSt
the resulting phenotype is cyclopia in the embryonic head.
Expression of rhohs.PSt
using multiple heat shocks during larval stages leads to failure of photoreceptor differentiation and a dorsoventral stripe of scar tissue in the adult eye.
Embryos overexpressing rhohs.PSt
show a 'cyclops' phenotype in which the optic lobes are enlarged and show dorsal fusion.
Heat shock driven misexpression of rhohs.PSt
produces a number of wing phenotypes including, blisters separating the dorsal and ventral surfaces of the wing, ectopic crossveins, an ectopic vein spur running between wing veins L3 and L4 near the margin, and a thickened L3 vein. All phenotypes are seen if heatshock occurs within 0-30 hours after puparium formation (APF).
Ubiquitous and sustained expression of rhohs.PSt
under heatshock, results in supernumerary midline glial cells.
Overexpression of rhohs.PSt
results in dramatically enlarged wing vein tissue.
Causes complex deformity of the embryonic visual system. Optic lobe is enlarged and invaginates earlier and at a more dorsomedial position than in wild type. The differentiation of Bolwig's organ is also abnormal; in many cases it does not separate from the optic lobe and does not form axons. Heat shock activation between 5 and 7 hours postfertilization has the strongest effect.
Shows extra wing vein material phenotype, even at 25oC.
Causes dorsalization of the egg.
Heat shocked embryos show an increase of 1 or 2 chordotonal organs in the lateral pentascolopidial chordotonal organs (LCh5) and in the ventral cluster.
The number of midline glia cells is increased to an average of 7 cells per segment in homozygous embryos.
Ectopic expression of rhohs.PSt
in the disc and pupal wing results in the differentiation of ectopic and thicker veins.
Heat induced expression causes an increase in the number of chordotonal neurons.
The number of MGA and MGM cells can be increased by the ectopic expression of rho
. Onset of midline glial cell death is shifted earlier, to stage 12 rather than stage 13, in these embryos.
Heat shock at germband extension leads to the production of stretch receptor organ precursor cells and heat inductions during wing vein development leads to the formation of ectopic veins.
Eggs laid after heat shock have dorsalized eggshells and give rise to dorsalized embryos, with expansion of dorsal structures at the expense of ventral. In some embryos stronger dorsalization was detected in the anterior region than the posterior, similar to the mutant phenotype in fs(1)K10 mutants. The large percentage of nonhatching embryos reflects failure of fertilization and dorsalization of the embryo.