lamina & neuron
sensory neuron & axon & embryo
The supernumerary cone cells in pupal retina observed in either Vav2 or Vav3 mutants is almost completely suppressed by combination with spi1 in heterozygous state but the increased number of primary pigment cells remains unchanged.
vnL6 enhances the ventral patterning defects seen in spi1 mutant embryos. The double mutants have a reduced number of denticle belts compared to controls, fusion of the denticle belts and an anterior hole. The phenotype is further exacerbated by Krn27, with embryos having no denticle belts and a large anterior hole. A zygotic grkHF mutation has no additional effect.
Krn27 enhances the ventral patterning defects seen in spi1 mutant embryos. The double mutants have a reduced number of denticle belts compared to controls, fusion of the denticle belts and an anterior hole. The phenotype is further exacerbated by vnL6, with embryos having no denticle belts and a large anterior hole. A zygotic grkHF mutation has no additional effect.
Krn27/Krn9 enhances the wing vein phenotypes seen in vnL6/vn1 mutants. A greater proportion of flies show longitudinal vein 3 loss than in vnL6/vn1 alone. The phenotype is further enhanced by one copy of spi1.
The extra wing vein phenotype caused by expression of CG4096KK108644 under the control of Scer\GAL4Act5C.PU is significantly suppressed if the also simultaneously carry both spi1 and Krn27. The suppression is more pronounced if the flies simultaneously carry spi1, Krn27 and vnL6.
spi1 clones made in the Df(3L)Krn260 background in third instar eye discs show irregular spacing of R8 cells, cell clustering defects behind the furrow, and contain large numbers of cells undergoing apoptosis.
Expression of CycEScer\UAS.cLa, under the control of Scer\GAL4en-e16E, in spi1 embryos increases cell death in the posterior compartment, relative to expression of CycEScer\UAS.cLa in a wild-type background.
The increase in the number of midline glia per ventral nerve cord segment seen in embryos expressing jingScer\UAS.cSa under the control of Scer\GAL4sli.PS is not suppressed by spi1, but expression of jingScer\UAS.cSa under the control of Scer\GAL4sli.PS in a homozygous spi1 background does not induce extra midline glia and the number of midline glia per ventral nerve cord segment in these double mutant embryos is reduced compared to wild type and is similar to that seen in homozygous spi1 single mutants. The rough eye phenotype caused by expression of jingScer\UAS.cSa under the control of Scer\GAL4GMR.PF is dominantly suppressed by spi1. jing01094/spi1 double heterozygous embryos have a reduced number of midline glia per ventral nerve cord segment compared to wild type. jing3/spi1 double heterozygous embryos have an increased number of apoptotic cells in the CNS midline at stage 12 compared to wild type (where cell death is uncommon at this stage). jing3/spi1 double heterozygous embryos have breaks in the dorsal trunk of the tracheal system at stage 15.
The loss of midline glial (MG) cells in spi1 homozygous embryos is suppressed by WrvX1/WrvX1. Approximately twice as many MG cells survive as in wild-type (average of 5.7 per segment n=133, compared to average = 2.8 for wild-type).
salm3 spi1 double mutant embryos have an average of 3 +/- 0.08 neurons per lch5 organ, similar to spi1 single mutant embryos. The embryos show misplacement of the lch5 organ along the dorsoventral axis comparable to the phenotype seen in salm single mutants.
spi1 ; vnunspecified double homozygotes have one dorsal midline cell per segment and a reduction in the number of ventral neurons. The effect on the dorsal midline cells appears to be additive, while the effect on the number of ventral neurons suggests a genetic interaction between spi and vn. Most spi1 ; vnunspecified double homozygotes show complete fusion of the commissures and complete loss of the longitudinal tracts. Some embryos lack both longitudinal and commissural connectives, with most axons remaining within one hemi-segment. vnunspecified homozygotes that are also heterozygous for spi1 have a single fused commissure and variably reduced longitudinal connectives.
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.
Reduction in dose of spi rescues the rhohs.sev eye to a near wild-type phenotype; regular array of ommatidia, regular arrangement of photoreceptors and unbroken lattice of pigment cells. Rescue is not always complete. Reduction of the dose of spi causes some suppression of the EgfrE3 rough eye phenotype; more ommatidia and increase in the size of the eye.
Animals heterozygous for spiSCP2 and spi1 which have been rescued by spiScer\UAS.cSa with Scer\GAL4hs.PB to the third instar stage show relatively normal ommatidial development at the posterior of the eye imaginal disc. More anterior columns of ommatidia have reduced photoreceptors. In the lamina, retinal projections appeared normal but LPCs show no neuronal differentiation. This phenotype is rescued by the introduction of Scer\GAL4GMR.PF or in clones induced to produce Scer\GAL4αTub84B.PP.