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 gene. 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]