Worm Breeder's Gazette 7(1): 91

These abstracts should not be cited in bibliographies. Material contained herein should be treated as personal communication and should be cited as such only with the consent of the author.

A Deficiency of the Left Half of unc-22 IV causes Dominant Twitching

T. Rogalski, D. Baillie

Figure 1

The mutation s290 was picked up as a dominant twitcher after 
formaldehyde mutagenesis of N2 worms (Moerman and Baillie, 1981).  
This mutation is lethal when homozygous, blocking at an early larval 
stage (D.  Moerman, personnel communication).
Although allelism tests could not be done, it was possible to show 
that the twitcher phenotype is due to a defective unc-22 gene.  s290 
was positioned with respect to two alleles of the unc-22 gene by 
intragenic recombination mapping.  These two alleles, s8 and s12, 
represent respectively the left and right boundaries of the unc-22 
fine-structure map (Moerman and Baillie, 1979).  s290 maps 
approximately 0.004 map units (6 recombinants/565,500 total progeny) 
to the left of s12.  This result places s290 near the middle of the 
unc-22 fine-structure map.  However, no recombinants were observed (
283,650 total progeny) from unc-5(e152)unc-22(s8)dpy-4(e1166)/s290 
hermaphrodites, placing s290 near the left end of the gene.  These 
mapping results can be explained if s290 is a deficiency breaking in 
the middle of the unc-22 gene and extending to the left end of this 
The lethality of s290 homozygotes can be explained if this mutation 
is a deficiency extending into essential genes adjacent to the unc-22 
gene.  Complementation tests were done between s290 and four essential 
genes, let-56, let-65 and let-59, which map 0.01 0.
2, 0.4 and 0.6 map units respectively to the left of unc-22 (see map 
below).  Hermaphrodites with the genotype, s290 IV/ +; dpy-11 V, were 
mated to let-x s.  Since s290 is dominant, 
the outcrosss Unc-22 worms had to be progeny tested to determine 
whether their genotype was s290/ +; dpy-11/ + or s290/ let-x 
dpy-11/ +.  If none of the outcrossed Unc-22 
progeny from a particular cross carried the let-x 
me, then that let gene is uncovered by s290.  
s290 failed to complement only let-56, the closest known let gene (
68/68 Unc-22 progeny were s290/ +; dpy-11/ +).  Therefore s290 appears 
to be a deficiency breaking inside the unc-22 gene and extending into 
at least one essential gene to the left of unc-22.If the dominant 
effect of s290 is due to the presence of an incomplete unc-22 peptide, 
then the deficiency hypothesis indicates that it is the right half of 
the gene that is being transcribed and translated.  The most appealing 
explanation to account for this is that the unc-22 gene is transcribed 
from right to left on the genetic map.
[See Figure 1]

Figure 1