Heterozygotes show resistance to dietary α-methyl dopa. 48.3% of Tcr40/Tcr45 individuals die during embryogenesis. These animals live for 48 or more hours after egg deposition but fail to escape from the egg. They appear as mature first instar larvae with an underpigmented cephalopharyngeal apparatus. 7.5% of Tcr40/Tcr45 individuals survive past adult eclosion, but these adults are usually found dead or dying in the food. Adults not found in the food are unable to walk on their tarsi and walk on their metatarsi or tibia with uncoordinated leg movements. Both pharate and eclosed adults have a range of abnormalities, including dark, rough, often reduced eyes with black spots, missing bristles (especially from the head), one to all ocelli missing, notching of the wings, reduced scutellum, Minute-like bristles mixed with wild-type bristles, unexpanded ptilinum, reduced sex combs and a greyish abdomen.
Tcr/+ heterozygotes resistant to dietary α methyl dopa. Homozygous lethal. Heteroallelic combination Tcr40/Tcr45 partially lethal, 48.3% dying as late embryos, these unhatched larvae having underpigmented mouthparts like lethal Ddc/Ddc embryos; only 7.5% go through pupation and manage to eclose, but these adults die soon. Both pharate and hatched adults have cuticular abnormalities involving the eyes (rough, often small, with black, necrotic spots), ocelli (often missing), wings (notched), scutellum (reduced), bristles (missing or M-like), sex combs (reduced) and abdomen (grayish). Tcr/+ heterozygotes suppress the lethality of amd heteroallelic combinations; Tcr heteroallelic combinations are not rescued genetically by amd/+, but show increased embryonic mortality as a maternal effect of amd.
amd5/amd1, amd6/amd1 or amd11/amd1 flies show an increase in viability when they are also heterozygous for Tcr40. Complementation between Tcr40 and Tcr45 is not increased by amd1 or amdH26, but these amd alleles have a maternal effect on Tcr40/Tcr45 embryos, causing an increase in embryonic mortality.
partially complements Tcr45