An Hsp70 promoter drives expression of a wild-type rho cDNA.
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.
Rough eye phenotype.
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.
Scer\GAL4en-e16E, mskUAS.cLa, rhohs.PSt has abnormal size | adult stage phenotype
Scer\GAL4en-e16E, rhohs.PSt has wing vein | ectopic phenotype, suppressible by Scer\GAL4en-e16E/mskUAS.cLa
rhohs.PSt has dorsal appendage phenotype, suppressible by spi1
rhohs.PSt is an enhancer of adult optic lobe | adult stage phenotype of vap2
rhohs.PSt is a non-enhancer of phenotype of Egfrflb-2E07
rhohs.PSt is a suppressor of midline glial cell phenotype of spi1
rhohs.PSt is a non-suppressor of phenotype of Egfrflb-2E07
Scer\GAL4en-e16E, mskUAS.cLa, rhohs.PSt has wing phenotype
rhohs.PSt, spi1 has larval longitudinal connective phenotype
The extra veins in the adult wing induced by rhohs.PSt are strongly suppressed by the addition of ectopic mskScer\UAS.cLa (under the control of Scer\GAL4en-e16E). rhohs.PSt mskScer\UAS.cLa (under the control of Scer\GAL4en-e16E) wings are significantly larger than rhohs.PSt wings, despite no decrease in cell density, indicating an increase in cell division.
When rhohs.PSt; spihs.PG flies are exposed to heat shock, no effect of elevated spihs.PG expression is seen beyond that attributable to rhohs.PSt misexpression. When Shs.PK; rhohs.PSt; spihs.PG are exposed to during early pupariation (mostly between 6 and 12 hours after puparium formation (APF)) a phenotype is seen that is stronger than Shs.PK; rhohs.PSt alone. Also, in contrast to the diffuse ectopic veins induced by Shs.PK ; rhohs.PSt, a sharp pattern of well defined forked longitudinal veins is observed. A phenotype can also be seen in the eye, in which cell death is localised at the anterior part of the eye, when heat shock is provided between 0 and 6 hours APF.
The ubiquitous expression of rhohs.PSt under heatshock leads to a partial suppression of the spi1 loss of midline glial cell phenotype. No significant suppression of the axon tract phenotype is seen, however longitudinal tracts are thinner in these embryos. (this effect is not seen when rhohs.PSt is added to wild-type embryos). Commissure separation in rhohs.PSt,spi1 is not improved. The ubiquitous expression of rhohs.PSt under heatshock has no effect on SIIN or Egfrflb-2E07 embryos.
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