Homozygous mutants are sluggish after hatching and die at the end of the first instar larval stage.

Homozygous follicle cell clones do not affect cell proliferation or viability.

Homozygous follicle cell clones show prominent epithelial defects, including stacking of follicle cells and a multilayering phenotype of more than three layers of cells (38% of clones) and flattening or stretching of the follicular epithelium (42% of clones). The remaining 20% of clones show swelling.

Homozygous follicle cell clones already show disorganisation or loss of microtubules in pre-stage 6 egg chambers. Loss of microtubules along the lateral cortex becomes more obvious in later egg chambers containing homozygous clones.

Vhl¹ homozygous females which have been rescued to adulthood by expression of Vhl^{Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^btl.PS are sterile, with 70% of the ovarioles containing only degenerated egg chambers. The remaining ovarioles have very severe epithelial defects in their egg chambers, including prominent expansion of the epithelium into the germ cell proper. In other cases, the entire follicle cell epithelium becomes multilayered and the nurse cell complex is collapsed. Microtubules are barely detectable in the mutant egg chambers.

Embryos derived from females carrying homozygous germline clones mated to heterozygous males do not hatch and show a complete failure of tracheal formation.

Homozygotes are sluggish after hatching but can feed and survive until the end of the first larval instar. No homozygotes survive past the second instar stage.

Mutant embryos show two distinct classes of mutant tracheal phenotypes; the first involves abnormal tubule migration and the second involves enlarged tracheal lumens and tortuous tracheal tubes. Embryos having both classes of phenotype are seen.

The abnormal tracheal tubule migration phenotype includes misdirected tubules and ectopic branching in addition to disruption of the dorsal trunk. This phenotype is seen in heterozygous embryos (56% of heterozygotes show moderate defects, 6% show severe defects) as well as in homozygous embryos, where the phenotype is more severe (65% of homozygotes show moderate defects, 35% show severe defects). In some mutant embryos an entire section of the dorsal trunk migrates dorsally or ventrally. Abnormal sprouting of filopodium-like projections can be seen in isolated cells. In very severe cases, the entire tracheal system is disrupted, with an abundance of ectopic branching and rounded tracheal cells detached from the epithelium.

The enlarged tracheal lumen phenotype includes tracheal tubules with tortuous paths and dilated dorsal trunks. The phenotype is seen in both heterozygous (63% of cases) and homozygous embryos. Stage 14 mutant embryos show appearance of luminal chitin (as occurs in wild type), but stage 15 mutant embryos show a defect in the clearance of luminal chitin that normally occurs at this stage (chitin remains abundant in the mature dorsal trunk and is filled up to the apical surface of the tracheal cells in the mutant embryos).

Vhl¹ has increased mortality during development phenotype, suppressible | partially by Scer\GAL4^Tub.PU/Hsap\VHL^19.UAS

Vhl¹ has increased mortality during development phenotype, suppressible | partially by Scer\GAL4^Tub.PU/Hsap\VHL^30.UAS