Worm Breeder's Gazette 10(3): 128

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.

Interaction of Vulvaless Genes: Hyperinduction and Allele-specific Interactions

Gregg Jongeward and Paul Sternberg

Figure 1

Figure 2

In wild-type hermaphrodites, three of six Pn.p cells are induced to 
divide and generate vulval cells by a signal from the anchor cell.  
Fewer cells are induced in most worms carrying Vulvaless (Vul) 
mutations such as let-23(syl), 53, sy2, el309) and 
lin-7(el413, n760).  However, the alleles let-23(nlO45), 
8, nlO5, nl67) and lin-7(n308, n701) result in a 
hyperinduced (Hin) phenotype.  Specifically, worms homozygous for any 
one of these mutations average more than three Pn.p cells induced.  
This hyperinduction correlates with 'blips' near the vulva in egg-
laying proficient (Egl+) worms.  For let-23(nlO45), this seems to be 
caused by a slight decrease of let-23 activity [see Aroian and 
Sternberg, WBG 10(2)].  This hypothesis is based on the observations 
that nlO45/Df is tightly Vul and that a Hin phenotype can be recreated 
in a let-23(syl)/1et-23(mn224) heterozygote.  (syl is a Vul non-lethal 
allele while mn224 is a lethal allele which partially complements the 
Vul defect).  Of these heterozygotes, 20% are Hyperinduced and 80% are 
wild type.  According to the current hypothesis, this lower activity 
is sufficient to respond to the inductive signal but not capable of in 
turn activating the 'Lateral Inhibitory Signal' [Sternberg WBG10(1)] 
which prevents more than three cells from responding to the signal.
To further examine this hypothesis, we have examined the 
interactions between Hin alleles of let-23, 
tructed a set of double mutant 
strains carrying two Hin mutations.  If the Hin phenotype of these 
strains is due to a lower level of activity, then a Hin; Hin double is 
predicted to have a Vul phenotype.  Alternatively, if Hin is due to a 
heightened response to the inductive signal, then the double mutants 
should display a more extreme phenotype.  As internal controls, we 
also constructed Hin; Vul doubles and Vul; Vul doubles.  These strains 
also allowed us to determine whether there are any gene-specific or 
allele-specific interactions.
As a measure of the level of induction, we have scored the number of 
Egl+ worms with one or more blips near the vulva divided by the total 
number of worms.  For instance, a lineage such as 322123 or 332122 
would be Egl+ with a blip, 322122 Egl+ with two blips (1, 2, and 3 
refer to the primary, secondary and tertiary lineages; the underlined 
cells would form the vulva).  The lineage 321123 is wild type at the 
plate level.  This measure could also include some Vul animals with 
lineages such as 331323.  Using this test, let-23(nlO45) at 20  is 19% 
Hin, lin-2(n768) is 25%, and lin-7(n308) is 12%.  We have set 10% as 
an operational definition of Hin.  Of the seven Hin; Hin doubles that 
have been scored the highest score was less than 3%.  These 
observations support the hypothesis that Hin alleles are hypomorphic.
[See Figure 1]
We have observed allele-specific interactions between lin-2 and lin-
7.  Two of the three Hin alleles tested, lin-2(n105) and lin-2(n768) 
decrease the penetrance of Vul alleles lin-7(e1413) and lin-7(n760), 
but the Hin allele lin-2(n167) does not suppress any of the Vul 
alleles tested.  All of the other doubles are essentially Vul.  We 
speculate that the lin-2 and lin-7 gene products interact directly.  
In addition, any double made with let-23 (n1045) is very tightly Egl- 
with little, if any, hyperinduction, consistent with the hypothesis 
that let-23 acts at a different step than lin-2 and lin-7.[See Figure

Figure 1

Figure 2