Worm Breeder's Gazette 10(1): 98

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Intragenic Mapping of unc-26(IV)

D.L. Charest and D.L. Baillie

Figure 1

Individuals homozygous for an unc-26 mutation are severely paralyzed 
even though the muscle appears normal (Waterston et al.  1980).  
Because of the interesting nature of this phenotype, we have 
undertaken the study of the unc-26 gene.  unc-26 is located on the 
right arm of LGIV, but lies outside the intensively studied unc-22 
gene cluster region.  A partial fine structure map of the unc-26 
alleles has been constructed.
Presently, there are eleven alleles available for our study:  e176, 
e205, e314, e345, e429, e446, e568, and e1048 were isolated from 0.05 
M EMS mutagenesis (Brenner 1974), while e1196 and m2 were induced with 
ICR 191 (Riddle and Baillie) and DES (D.  Riddle) respectively.  e1710 
was isolated in our laboratory in a mut-4 background (kindly supplied 
by D.  Moerman) and probably resulted from a Tc1 insertion.  The 
method used for fine structure analysis was modified from Moerman and 
Baillie (1979).  Triple mutant hermaphrodites of the genotype unc-22 
ssed to unc-26(y)/+ males.
The resulting heteroallelic hermaphrodites, unc-22  
unc-26(Y) +, self-fertilized and the second 
generation was screened for exceptional individuals.  Figure 1 shows 
the relative positions of the alleles tested so far.  The largest 
recombinational map distance is 0.025 map units.  The remaining 
alleles are now being positioned on the map.
The alleles display variations in the severity of their paralysis.  
For this reason we are investigating the effect of each mutation in 
the hemizygous state over the deficiencies sDf21 and nDf27 (from R.  
Horvitz).  The informational suppressor sup-7 (Waterston 1980) is 
being used to identify alleles within the coding region.  Also, work 
is in progress to isolate the Tc1 flanking sequences in e1710.  Please 
note that we would appreciate receiving any unc-26 alleles not listed 
[See Figure 

Figure 1