Worm Breeder's Gazette 10(2): 78

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.

With our Complements . . . sqt-3, rol-4 and lon-3

Richard Espey and Kaye Edwards

Figure 1

To understand the role of the sqt-3 gene in C.  elegans cuticle 
development, we have constructed allelic combinations with known 
alleles of sqt-3(sc63, e24), rol-4(sc8, sc42, and b238), lon-3 (e2175) 
and ctDf1.  To obtain progeny of type a/b, N2 males were crossed with 
a/a hermaphrodites to give a/+ males.  These were mated to b/b 
hermaphrodites at 25 C to give a/b hermaphrodites among others.  
Suspected a/b worms were confirmed by allowing them to self at 25 C, 
and a resulting 1:2:1 segregation of a/a : a/b : b/b confirmed the 
[See Figure 1]
'-' indicates the cross was not performed.  All rollers (R) are left 
rollers.  Weak rollers(wR) were classified by their occasional 
twisting, particularly when prodded, and by their visibly twisted 
cuticle.  Strong dumpy(xD) worms range from being slightly larger than 
eggs to about 50% N2 length, with a correspondingly wide range of 
mobilities.  All alleles of rol-4 are recessive, as is sqt-3(e2117).  
The other two alleles of sqt-3(sc63 and e24) have dominant phenotypes (
roller and weak dumpy) as does ctDf1 which is a weak long (wL).  
Phenotypes not in bold face were obtained from Kusch and Edgar, 
Genetics 113: 621-639, 1986, or from Cox et al., Genetics 95: 317-339, 
If sqt-3 and rol-4 are different genes, the expected phenotype of 
the heteroallelic combinations would be either wild type or the 
phenotype of the dominant sqt-3 allele.  An exception to this would 
arise in the case of intergenic noncomplementation, which has been 
seen for other cuticle defective mutations.  Our results show that in 
many cases the combination of a sqt-3 allele and a rol-4 allele, both 
in heterozygous configurations, generates a doubly mutant phenotype.  
This phenotype is the combined display of what both alleles would show 
alone were they homozygous.  For example, e2117/sc42 is a severe dumpy 
e2117/b238, e24/sc8, and e24/sc42.  In contrast, sc63, the only true 
sqt allele (m/m = Dpy; m/+ = Rol) is suppressed by the two rol-4 
alleles tested: sc63/sc8 is WT and sc63/sc42 is a weak roller.
We have also determined that the phenotype of rol-4(sc8)/ctDf1 is a 
weak roller, suggesting that it is located within the ctDf1 region.  
If sc8 were not located in the deficiency, the expected phenotype 
would be a weak long, barring extragenic effects.  This contradicts 
the assignment of rol-4 to the right of ctDf1 as is illustrated on the 
genetic map, 1987.  We have no data that support the notion that sqt-3 
and rol-4 are separate loci, although we have not yet determined the 
frequency of recombination between sqt-3 the assignment of these 
depend on sequence data of and rol-4 alleles.  Ultimately, alleles to 
one or the mutant DNAs.
Lon-3(e2175) may also be located in the ctDf1 region since 
e2175/ctDf1 is a weak roller, not WT like e2175/+.  Lon-3(e2175) does 
not interact with any other allele tested, however, and is unlikely to 
be allelic with sqt-3 / rol-4.These complementation data allow us to 
predict the range of phenotypes that may be generated as additional 
mutations closely linked to sqt-3.  We are beginning to generate new 
mutations that fail to complement sc63 using [32P] as the mutagen.  
Such new mutations are likely to have DNA alterations detectable by 
Southern blotting (Hoskins et al., WBG 10, No.  1).  We will probe 
these mutant DNAs with the collagen genes which we have isolated from 
the myo-3 contig (Edwards, WBG 10, No.  1).

Figure 1