Enhancer of sda mutations
Line | Paralysis sda/+ (%) | Paralysis BS (%) | Description | P site | Candidate gene |
---|---|---|---|---|---|
A | 100 | 100 | BS | 86B | Helix-loop-helix protein; insertion is 80 bp upstream of gene |
B | 47 | 0 | Enhancer | 85D | Transketolase; insertion in promoter of gene |
C | 46 | 0 | Enhancer | 51F9 | DNA mismatch repair protein; insertion is 1.7 kb upstream of promoter |
D | 66 | 84 | BS | 59A | Filamin actin-binding protein; insertion in third intron of gene |
F | 93 | 33 | BS | 47F | Translocation protein; insertion in or near putative exon region |
G | 53 | Lethal | Enhancer | 89B | Glycoprotein; insertion in first intron of gene |
H | 75 | Lethal | Enhancer | 68F | Spermidine synthase (CG17155); insertion is 3 kb from gene |
I | 85 | Lethal | Enhancer | 61D | Casein kinase I |
J | 83 | 60 | BS | 88A | Zinc-finger protein with tudor domains |
L | 63 | 0 | Enhancer | 86D | CG4800 similar to translationally controlled tumor protein |
M | 40 | 0 | Enhancer | 75C | CG12477 |
N | 87 | Lethal | Enhancer | 90D | RNA-binding protein; insertion in promoter |
O | 78 | 10 | BS | 41C | No 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.