Heterozygotes show normal resistance to infection with P.aeruginosa by septic injury.
Rho172R mutant embryos exhibit a defect in tracheal invagination.
Clones of Rho172R in eye discs show malformed ommatidial preclusters.
Stage 17 Rho11B/Rho172R embryos show partial disruption of the cortical actin cytoskeleton in the spiracular chamber.
Rho172O/Rho172R embryos exhibit dramatic defects in head involution. None of these mutant embryos have a clear dorsal hole, although they frequently show puckering or segment misalignments along the closed midline seam. During dorsal closure lamellipodial and filopodial protrusions are more abundant at the leading edge than in wild-type, significantly increaing the total protrusive area of the leading edge. The cytoskeletal architecture typical of the leading edge is lost.
Laser wounded Rho172R/Rho172O embryos fail to assemble a continuous actin cable in wound-edge cells and there is little or no initial contraction of the leading edge of these cells. The leading-edge extends filopodia that are longer (extending up to 12 μm) and approximately three times more common than in wild-type embryos. In many instances, several filopodia coalesce to form a lamellipodium. Lamellipodia from adjacent leading-edge cells apparently tug on one another, resulting in the formation of several local zipping fronts around the wound margin, a behaviour only observed in wild-type in the last moments of wound closure, when opposing epithelial fronts are driven close enough together. Despite these differences with the wild-type, Rho172R/Rho172O embryos are able to close their wounds, but these take on average almost twice as long to repair as in their wild-type counterparts. There is a lag phase of nearly 2 hours (the time in which an equivalent wild-type wound can close fully) before the disorganized leading edge begins to move forward significantly. During this initial period, no obvious changes in cell shape occur in the leading-edge epithelial cells. However, once forward movement begins, the wound closes at a rate that is not significantly different to that of a wild-type wound (7.0+/-1.9 μm2/min; n = 6 in the mutant compared with 9.0+/-2.6 μm2/min; n = 5 in the wild type).
Mushroom body neuroblast clones homozygous for Rho172R consistently contain about 10-12 cells in third instar larvae (in contrast to wild-type mushroom body neuroblast clones which contain more than 150 neurons). Within each mutant clone, two of the nuclei are much larger than the rest of the nuclei. The clones project extensive dendrites in wandering third instar larvae that appear to occupy the entire calyx region. The effect on dendrite growth appears to be autonomous. In adulthood, mutant clones still contain 10-12 cells with axons projecting to only one medial lobe, in contrast to wild-type clones, which contain over 500 neurons that project axons to five lobes. Neurons of two cell or single cell mushroom body neuroblast clones homozygous for Rho172R and generated in newly hatched larvae have axon projections that are indistinguishable from wild type.
In homozygous mutant embryos, cytokinesis is blocked in affected cells. Many cells in the head region of the embryo become polyploid and contain two nuclei per cell. In addition polyploid cells are occasionally found in thoracic or abdominal segments of mutant embryos. Homozygous mutants have an "anterior open" phenotype.
Rho172F/Rho172O, Rho172F/Rho172R and Rho172R/Rho172O embryos have an "anterior open" phenotype; the epidermis fails to close in the dorsal/anterior region. Rarely, the dorsal epidermis also fails to close. Some head structures are missing.