Worm Breeder's Gazette 11(4): 75

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.

sup-9(n1550) -- A New Rubberband Mutation

Joshua Z. Levin and Bob Horvitz

sup-5 is a member of a group of interacting genes (unc-93, sup-9, 
sup-10, sup-11, and sup-18) involved in muscle structure and function. 
unc-93(e1500), 00), and sup-10(n983) are rare, 
altered-function mutations that confer a distinctive uncoordinated (
'rubberband'), muscle-defective phenotype.  When a rubberband mutant 
is prodded on its head, the worm contracts and then relaxes without 
moving backwards, while a wild-type worm simply moves backwards.  This 
rubberband phenotype suggests that the worm can contract its muscles 
but that the regulation or coordination of the contraction is 
defective.  Null alleles of unc-93, sup-10, and 
sup-18 result in a wild-type phenotype alone and are recessive 
suppressors of e1500 and n983.  The wild-type null phenotype of four 
of these five genes suggests they may be functionally redundant.  
Certain rare alleles of sup-11 (including n403) act as dominant 
suppressors of unc-93(e1500) and recessive suppressors of sup-10(n983);
the sup-11 null phenotype is embryonic lethality.  Our model for the 
interaction of these genes is that the rubberband mutations produce 
abnormal gene products that disrupt a redundant process in the 
regulation of muscle contraction, but the absence of the gene products 
of four of these genes does not adversely affect muscle contraction.
A new rubberband mutation, n1550, was isolated by M.  Herman in an 
unrelated screen.  n1550 is the strongest rubberband mutation 
identified.  It has a dominant uncoordinated phenotype and a recessive 
phenotype of extreme sluggishness, very slow growth, and the 
production of few, if any, progeny.  We have assigned n1550 as an 
allele of sup-9 based on two observations.  First, n1550 maps to the 
same region of chromosome II as does sup-9 (by two-factor data with 
lin-31 II and being uncovered by nDf3).  Second, an F1 reversion 
screen of n1550 yields sup-9 null alleles.  (We screened for wild-type 
F1 progeny from EMS-mutagenized sup-9(n1550); 500 
n1415) dpy-17(e164) hermaphrodites mated with lin-42(n1089)/+ males.) 
Because reversion of the Unc phenotype associated with n1550 results 
in cis-dominant sup-9 null mutations and sup-9 null mutations do not 
suppress n1550 in trans, this experiment indicates that n1550 is an 
allele of sup-9.The pattern of suppression for sup-9(n1550) is as 
(1) n1550 is completely suppressed by an unc-93(0) mutation.  
(2) n1550 is completely suppressed by a sup-10(0) mutation.  
(3) n1550 is partially suppressed by a sup-18(0) mutation.  
(4) n1550 is not suppressed by sup-11(n403).  
This suppression pattern differs from that for the other rubberband 
alleles because n1550 is not suppressed by sup-11(n403).  n1550, like 
unc-93(e1500), is only partially suppressed by sup-18; by contrast, a 
weaker rubberband allele, sup-10(n983), is fully suppressed by sup-18.  
All the extragenic suppressors of n1550 act semi-dominantly, 
suggesting a stoichiometry among these gene products .
The identification of a rubberband allele of sup-9 provides further 
evidence that sup-9 participates in the same process(es) as do unc-93 
and sup-10.  Since unc-93 encodes a protein that appears to be 
membrane associated (Levin, J.  Z.  and Horvitz, B., CSH C.  elegans 
Meeting Abstracts 1989, p151), we propose that these three genes 
produce gene products that are likely to interact as a protein complex 
in the muscle membranes.