Imprecise excision of the P{PZ}sinu06524 element, resulting in a deletion of all the amino acids of the sinu open reading frame, without affecting the coding sequences of adjacent genes.
Mutant embryos have elongated trachea.
Stage 17 homozygous embryos show loss of the blood brain barrier (assayed by studying dextran uptake in living embryos).
The transepithelial diffusion barrier is compromised in homozygous embryos; a 10kD dye injected into the body cavity crosses the salivary gland epithelium in mutant embryos (in contrast to wild-type embryos). Numerous, well-differentiated septa are present in the cells of trachea, epidermis and salivary glands in late stage 17 mutant embryos. However, the total number of septa is significantly reduced, there a fewer groups of septa and the septa are not organised into continuous circumferential ribbons. Septa remain localised to the apical half of the lateral plasma membrane and the zonula adherens appears normal. Tracheal cells show additional defects in addition to the disruption of the septate junctions; the taenidium shows a highly irregular folding pattern in mutant embryos, in contrast to the regular pattern seen in wild-type embryos. The mutant tracheal cells have an unusually large number of vesicles in the cytoplasm.
Trachea in Nrx-IV4865 sinunwu7 double mutants have the same phenotypes as either single mutant. The tracheal defects of sinunwu7 mutant embryos are more severe in double mutant combination with nrv223B (expansion of the tube diameter is more severe in the transverse connective and visceral branches), vari03953b or convk06507b (severe diameter defects are seen in all multicellular branches and dorsal trunk length appears increased in both cases). sinunwu7 nrv2nwu3 double mutants have cyst-like structures in the tracheal ganglionic branches. The trachea of sinunwu7 scribj7B3 double mutants have the same phenotype as sinunwu7 single mutants.
sinunwu7 is partially rescued by Scer\GAL4btl.PS/sinuUAS.cWa