gt¹ larvae exhibit a prolonged third instar stage in 25% of females and 13% of male animals. Larvae and pupae are significantly larger than control animals.

In gt¹ larval brains, unilateral inneration of the prothoracic gland is observed, and an asymmetrically sized gland is observed in which the innervated portion is significantly larger than the non-innervated side. Cells on the non-innervated side contain nuclei that are significantly smaller compared to the innervated side.

There is an increase in the frequency of axon misrouting in gt¹ mutant larvae in the prothoracic gland. gt¹ mutants containing one or two prothoracic gland neurons in one of the brain lobes often show branching of axons at the base of the ring gland and innervation of both prothoracic glands. Similar branching defects are also observed in mutant brains where all four prothoracic gland neurons are present.

Delayed pupariation and enlarged larvae, pupae and adults.

gt^Q292/gt¹ larvae show a reduction in the normal inhibition of DNA synthesis following treatment with N-acetoxy-2-acetylaminofluorene. gt^13z/gt¹ larvae do not have a defect in the repair of X-ray induced DNA breaks.

Salivary gland chromosomes are double normal thickness in some cells.

Larval development is 4 days longer than normal, resulting in giant larvae, pupae, and imagos. Adult weight is 1.7 times normal. Not all genetically gt flies show the giant character, the rest have normal size. The distribution is sharply bimodal. The percentage of phenotypically giant animals is greatest in well-fed cultures, and is also raised by the modifying action of bb¹¹. RK3.