A nonsense mutation that results in the truncation of the GK domain in the expressed protein.
Amino acid replacement: Q?term.
The premature stop codon is predicted to eliminate the last thirds of the GUK domain without affecting the conserved putative GMP-binding residues.
Nucleotide substitution: C2752T.
C11405971T
C2752T
Q926term | dlg1-PA; Q928term | dlg1-PB; Q918term | dlg1-PD; Q918term | dlg1-PE; Q933term | dlg1-PG; Q869term | dlg1-PH; Q869term | dlg1-PK; Q904term | dlg1-PL; Q918term | dlg1-PN; Q941term | dlg1-PP; Q933term | dlg1-PQ; Q918term | dlg1-PR; Q918term | dlg1-PS; Q901term | dlg1-PT
Q?term
Stop codon is predicted to eliminate the last thirds of the GUK domain without affecting the conserved putative GMP-binding residues.
In mutant pI cells the onset of spindle rotation is delayed. Unlike the wild-type, rotation is observed in late metaphase.
Pharate adults exhibit severe bristle defects, antenna and legs have small overgrowth regions, eyes show defects in the planar polarity of the ommatidial bristles.
The lethal period is during the late pupal phase.
late pupal lethal
dlg1[+]/dlg118 is a non-enhancer of ommatidium phenotype of Vangstbm-153
dlg1[+]/dlg118 is a non-suppressor of ommatidium phenotype of Vangstbm-153
Heterozygosity for dlg118 has no effect on the frequency of ommatidia that show planar cell polarity defects in Vangstbm-153 homozygotes.
Perrimon.
Class III mutation.