C26088238T
C?T
Q151term | dysf-PB; Q187term | dysf-PC; Q187term | dysf-PD
Q187term
Nucleotide substitution: C?T.
Amino acid replacement: Q187term.
The premature stop codon is in the HLH region, resulting in a truncated 187 residue protein (as opposed to 917 residues), which lacks the PAS-1 and PAS-2 domains.
dysf2/dysf3 escapers display a complete absence of tarsal joint formation with a small shortening of the tarsal region. No defects are observed in most proximal joints or in the tarsus/pretarsus joint. The joint between the a5 and the arista in the antenna is also lost.
The distribution of apoptotic cells in the dysf2/dysf3 mutant prepupal leg is altered compared to wild type.
The ganglionic branches, dorsal branches, and lateral trunk branches in dys2/dys3 mutant second instar larvae show a complete absence of fusion in all branches examined. The dorsal trunk is fused and relatively normal in appearance, although some dorsal trunk fusion sites are constricted. Penetrance and expressivity are 100%.
In dys2/dys3 stage 16 embryos the dorsal branches and lateral trunks fail to fuse, while the dorsal trunk is fused.
dysf3/dysf2 has tarsal segment phenotype, non-suppressible by Nint.G.UAS/Scer\GAL4ptc.PU
dysf3/dysf2 has joint phenotype, non-suppressible by Nint.G.UAS/Scer\GAL4ptc.PU
dysf3/dysf2 is a non-suppressor of tarsal segment phenotype of Nint.G.UAS, Scer\GAL4ptc.PU
dysf3/dysf2 is a non-suppressor of joint | ectopic phenotype of Nint.G.UAS, Scer\GAL4ptc.PU
dysf2/dysf3 does not suppress the production of cuticle folds along the proximo-distal axis of the leg that resemble ectopic joints seen when Nint.G.Scer\UAS is expressed under the control of Scer\GAL4ptc.PU (and limited to the third instar larval stage using Scer\GAL80ts.αTub84B). As in dysf2/dysf3 mutants alone, endogenous tarsal joints are not formed.
