Imprecise excision of P{lacW}Tps1k08903 generates a 2331bp deletion, corresponding to amino acid resides 44-594 of Tps1. Tps1d2 lacks the entire TPS domain and an N-terminal part of the TPP domain.
Tps1d2 homozygotes do not show significant mortality or changes in body size during the larval stage.
Maternal and zygotic Tps1d2 mutants survive into the pupal period and exhibit identical lethality.
Tps1d2 mutant larvae exhibit almost undetectable levels of trehalose at the late third-instar larval stage.
Tps1d2 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, Tps1d2 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 Tps1d2 mutants exhibit minor but detectable defects in larval growth under normal food conditions.
Tps1d2 mutant flies do not exhibit differences in glycogen or TAG levels, while glucose levels are significantly reduced.
When their food contains low levels of protein but a normal level of glucose, Tps1d2 mutants display some lethality during the larval period, but many larvae survive to the pupal stage.
Tps1d2 is an enhancer of increased mortality during development phenotype of Glyp3-13
Glyp3-13, Tps1d2 has decreased body size | second instar larval stage phenotype
Glyp3-13, Tps1d2 has lethal - all die during larval stage phenotype
Tps1d2 is rescued by Tps1+tfull
Expression of Tps1+tfull, but not Tps1TPS or Tps1TPP, fully rescues the lethality and the decreased circulating glucose and trehalose levels observed in Tps1d2/Tps1d2 mutants.
