Tps1^k08903/Tps1^k08903 mutants exhibit lethality in the pupal stage and significantly decrease circulating trehalose levels in third instar larvae, as compared to controls, and these phenotypes are not rescued upon supplementation with trehalose feeding. Tps1^k08903/Tps1^k08903, but not Tps1^k08903/+, mutant larvae exhibit a decrease in hemolymph volume, and increased protein concentration in the hemolymph, but no significant difference in hemolymph osmolarity, and display significantly decreased viability after desiccation stress, as compared to controls. Tps1^k08903/Tps1^k08903 mutants do not exhibit any difference in glycogen levels after starvation or desiccation, as compared to controls.

Tps1^k08903 homozygous mutant clones in the eye have normal morphology at 1 day old and then show retinal degeneration.

Homozygous mutants of backcrossed Tps1^k08903 display lethality in the pharate adult, suggesting that a second-site mutation(s) in the original Tps1^k08903 line is responsible for the observed lethality at the early larval stage.

Tps1^k08903 mutant larvae grow at roughly the same rate as wild-type flies and undergo puparium formation similar to control flies. However, the body weight of these flies is ~9-12% lower than that of controls. Consistent with this, Tps1^k08903 mutant pupae are ~5-8% smaller. There is also a delay in the timing of puparium formation of ~10-12 hours. These results suggest that Tps1^k08903 mutants exhibit minor but detectable defects in larval growth under normal food conditions.

Tps1^k08903 mutant flies do not exhibit differences in glycogen or TAG levels, compared to controls, while glucose levels are significantly reduced.

Tps1^k08903 mutant larvae display a normal ingestion rate compared with control larvae.

Almost all Tps1^k08903 mutant larvae die after 1 day of starvation conditions (water-only), compared to 3 days for control flies. This lethality is completely suppressed by the addition of sucrose to the diet, indicating that Tps1^k08903 mutants are sensitive to the loss of sugar in their food.

Tps1^k08903 mutants show a significant reduction in the number of mitotic cells and an induction of apoptotic cells in the central nervous system after starvation.

Tps1^k08903 mutant larvae fail to grow and pupariate under conditions of low dietary sugar, although heterozygous Tps1^k08903 mutants survive into adulthood without any lethality. A two-fold increase in dietary yeast does not rescue the low-sugar diet-induced lethality found in these flies.

When their food contains low levels of protein but a normal level of glucose, Tps1^k08903 mutants display some lethality during the larval period, but many larvae survive to the pupal stage. However, mutant pupae are much smaller than in control pupae and the timing of puparium formation is significantly delayed.

A high sugar diet does not cause larval lethality in Tps1^k08903 mutants.

Tps1^k08903/Tps1^MI03087 transheterozygous mutants survive the larval period and die at the late pupal stage.

Tps1^k08903/Df(2L)BSC295 transheterozygous mutants survive the larval period and die at the late pupal stage.

Lethality occurs during the first instar.

Lethality occurs during third instar larval or pupal stages. Mutants do not show any visible disc abnormalities.