RopG27/RopG27 embryos display defects in the growth of the dendritic arbor in the dorsal class I and IV dendritic arborizing (da) neurons, including reduction in outgrowth of both primary dendrites and secondary lateral branches.
RopG27/RopG27 class IV da neurons in larval somatic clones first manifest defects (dendrites thinning) in dendritic growth at 72hrs after egg laying (AEL) and the phenotype (severely reduced dendritic complexity due to loss of branching, reduction in number of dendritic intersections, varicosities or terminal dendrites fragmentation) gets progressively worse at later stages of larval life, especially in terminal dendrites that show heightened sensitivity to loss of Rop. Axon growth of RopG27 mutant da neurons however appears normal until late in larval life (144hrs AEL) when axons show thinning and varicosities along the terminals.
Germ-line clones of this mutant often produce miniature eggs with greatly reduced surface volumes. Membranes in mature oocytes are also not intact.
Heterozygous larvae show a 35% decrease in the amplitude of the excitatory junctional potential in the muscle at the neuromuscular junction compared to control larvae, and a 79% reduction in miniature EJP frequency.
Embryos have little or no cuticle (epidermally derived structures are also abnormal), embryos fail to hatch into larvae. Trachea do not appear to be disrupted but they fail to fill with air in later embryos, possibly because they collapse due to insufficient cuticle deposition. Defects in the extracellular accumulation of secreted products was observed in other tissues: Malpighian tubules do not contain uric acid, the lumen of salivary glands contains severely reduced glue protein levels and the gut contents are incompletely digested due to lack of digestive enzymes. Morphology of the CNS is altered, fails to dissociate from the ventral epidermis and fails to shorten in mature embryos.