Single base deletion within the open reading frame, resulting in a frameshift and a premature stop codon.
Out of frame deletion predicted to result in a truncated Ret protein.
A 1bp deletion (A) in the second coding exon of Ret causes a frameshift and leads to a stop codon after two amino acids.
RetLM1 homozygous larvae as well as RetLM1/RetLM2 and RetLM1/RetLM3 transheterozygous larvae hatch normally hatch normally but show a range of feeding defects, as compared to controls: a foraging phenotype in which larvae move away from a central food source; accumulation of food in the oesophagus; reduced/absence of food in the midguts and absence of food in the oesophagus. In agreement, RetLM1 homozygous larvae show a similar frequency of proventricular contractions, but the wave of peristalsis is mostly absent. RetLM1 homozygous larvae are frequently immobile or sluggish in response to touch, as compared to controls.
RetLM1 homozygous embryos frequently exhibit missing or shortened frontal nerves as well as disrupted frontal ganglia and esophageal ganglia that do not migrate as far as in the control; axons enervating the larval midgut are tightly fasciculated crossing the proventriculus, but rapidly start branching on encountering the anterior midgut and do not project very far into the midgut.
RetLM1 has nerve | larval stage phenotype, non-suppressible by Scer\GAL4Ret.P2/SarmGD12314
RetLM1 has axon | larval stage phenotype, non-suppressible by Scer\GAL4Ret.P2/SarmGD12314
RetLM1 is partially rescued by RetUAS.Tag:FLAG,Tag:polyHis/Scer\GAL4Ret.P2