7bp (ACGTGTT) deletion within exon 4; frameshift mutation affects the C-terminal catalytic domain.
A 7bp deletion in Gpdh1 causes a frameshift and early translation termination.
Gpdh1A10/Gpdh1B18 is an enhancer of increased mortality during development phenotype of Ldh17/Ldh16
Gpdh1A10/Gpdh1B18, Ldh17/Ldh16 has abnormal developmental rate | second instar larval stage phenotype
Gpdh1A10/Gpdh1B18, Ldh17/Ldh16 has decreased body size | second instar larval stage phenotype
Gpdh1A10/Gpdh1B18, Ldh17/Ldh16 has abnormal size | second instar larval stage phenotype
Gpdh1A10/Gpdh1B18, Ldh17/Ldh16 has some die during first instar larval stage phenotype
Gpdh1A10/Gpdh1B18, Ldh17/Ldh16 has majority die during second instar larval stage phenotype
Gpdh1A10/Gpdh1B18, Ldh17/Ldh16 has larval brain | second instar larval stage phenotype
Ldh16/Ldh17, Gpdh1A10/Gpdh1B18 larvae show severe developmental defects: second instar larvae are much smaller and have a much lower body weight, as compared to either single transheterozygous condition and wild-type controls; 92-96h after egg-laying, larvae are still at L2, whereas either single transheterozygous condition and wild-type controls are already at L3; at L2 brains are much smaller and, even in size-matched larvae, presents significantly lower mitotic index, as compared to either single transheterozygous condition and wild-type controls; L2 posterior midguts are also much smaller than either single transheterozygous condition and wild-type controls.