TABLE 1

Enhancer of sda mutations

LineParalysis
sda/+ (%)
Paralysis
BS (%)
DescriptionP siteCandidate gene
A100100BS86BHelix-loop-helix protein; insertion is 80 bp upstream of gene
B470Enhancer85DTransketolase; insertion in promoter of gene
C460Enhancer51F9DNA mismatch repair protein; insertion is 1.7 kb upstream of promoter
D6684BS59AFilamin actin-binding protein; insertion in third intron of gene
F9333BS47FTranslocation protein; insertion in or near putative exon region
G53LethalEnhancer89BGlycoprotein; insertion in first intron of gene
H75LethalEnhancer68FSpermidine synthase (CG17155); insertion is 3 kb from gene
I85LethalEnhancer61DCasein kinase I
J8360BS88AZinc-finger protein with tudor domains
L630Enhancer86DCG4800 similar to translationally controlled tumor protein
M400Enhancer75CCG12477
N87LethalEnhancer90DRNA-binding protein; insertion in promoter
O7810BS41CNo obvious gene candidate
  • P elements were mobilized by dysgenesis in a sda/+ genetic background. Flies were tested for behavioral paralysis following mechanical (bang) stimulation and mutant lines selected on the basis of enhanced BS paralysis, that is, on the number of flies that paralyzed in the line [listed as “Paralysis sda/+ (%)”]. As indicated, some mutations (A, D, F, J, and O) caused BS paralysis when separated from the sda/+ background [listed as “Paralysis BS (%)”]. Transposon map positions were determined by in situ hybridization to polytene chromosomes. In each case, genomic DNA sequences flanking the P-element insertion site were sequenced. Listed are candidate genes that contain or are close to the transposon insertion site.