Imprecise excision of the P{SUPor-P} element in P{SUPor-P}TkR86CKG07724 has generated a 1,020bp deletion that removes most of the first exon of TkR86C, including the start codon and the first 60 amino acids which contain the signal peptide and most of the N-terminal extracellular domain ( 3R:6 ,576,803-6,575,782, release 5 coordinates). 678bp of the P{SUPor-P} element is still inserted at the chromosome break point.
1020 bp deletion in TkR86C resulting from the imprecise excsion of P{SUPor-P}TkR86CKG07724 removes most of the first exon of TkR86C. 678 bp of the P element remain.
Homozygous TkR86CΔF28 does not diminish baseline aggression in single-housed flies compared to controls.
TkR86CΔF28 is a suppressor of abnormal behavior | adult stage | heat sensitive phenotype of Scer\GAL4Tk, TrpA1UAS.(B).cKa
TkR86CΔF28, TkR99DMB09356 has abnormal behavior | adult stage phenotype
Homozygous TkR86CΔF28 significantly suppresses the aggression-promoting effect of activating neurons labeled with Scer\GAL4Tk (either the P{Tk-GAL4.TH}5Fa or P{Tk-GAL4.TH}3Ma insertion) through expression of thermosensitive TrpA1Scer\UAS.(B).cKa. This suppression is partially reversed upon expression of TkR86C+tCH322-17N40.
TkR86CΔF28, TkR99DMB09356 double mutants show a strong reduction in baseline and induced aggression compared to controls.