Worm Breeder's Gazette 15(3): 37 (June 1, 1998)

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 Between srf-6 and Dauer-Constitutive Genes

Laura J. Miceli, Samuel M. Politz

Department of Biology and Biotechnology, Worcester Polytechnic Institute, 100 Institute Road, Worcester, MA 01609

   Nematodes can alter their surface composition at the molts between
developmental stages.  Such surface alterations may enable parasitic
nematodes to evade immune attack during the course of infection.   We
are studying this phenomenon in C. elegans.  A specific surface epitope,
recognized by monoclonal antibody M37,  is normally expressed only at
the L1 stage.  Two classes of mutants, srf-6 and temperature sensitive
(ts) dauer -constitutive (daf-c),  have been identified which bind M37
at later larval stages.  This suggests that the srf-6 and daf-c genes
are involved in surface antigen switching.  
        Other than this phenotype, srf-6 mutants do not share any
phenotypes with the ts daf-c mutants.  Daf-c mutants grow continuously
at 16!C but form dauers at 25!C regardless of environment.  Most of the
daf-c genes encode components of a TGF-b like signaling pathway.
Grenache et al (Proc. Natl. Acad. Sci.USA, Vol 93, pp. 12388-12393, Oct.
1996)  showed that srf-6 appeared to act in surface antigen switching
independently of the dauer-defective gene daf-3, which encodes an SMAD
protein that is a downstream component of the TGF-b pathway.  This
suggests that srf-6 acts either in parallel with the daf-c genes or
downstream of daf-3 in the TGF-b pathway.  
        To identify possible genetic interactions between srf-6 and
daf-c genes, including the above possibilities,  double mutants
containing a combination of srf-6(yj13) with one of several alleles of
each daf-c gene were constructed.  We expected that if srf-6 and a
particular daf-c gene acted in parallel pathways, the double mutant
might  have a more severe phenotype for some aspect of surface antigen
switching or dauer formation.  Conversely, we expected that if srf-6
acted in the same pathway, downstream of the daf-c genes, the double and
single mutants would have similar phenotypes.
        Several unexpected results were obtained with a srf-6(yj13);
daf-4(m63) double mutant.  Almost 100% of srf-6(yj13); daf-4(m63) double
mutants form dauers at 16!C regardless of environment, while only 4%  of
the single daf-4(m63) form dauers.   daf-4 single mutants are small (the
Sma phenotype) but the srf-6(yj13); daf-4(m63) double mutants are
significantly smaller.  The srf-6(yj13);daf-4(m63) adult has an average
brood size of  38 (single mutant brood size is 135).  Under the same
conditions, an increase in dauer formation is also observed in the
srf-6(yj13); daf-14(m77) double mutants (5 % in the single, 55% in the
double).  Analysis of other srf-6(yj13);daf-c double mutants is
currently in progress.  
        The increase in dauer formation observed at 16!C in the presence
of srf-6(yj13) suggests a possible genetic interaction between srf-6 and
daf-c genes.  One interpretation of the severe phenotype observed is
that srf-6 and the daf-c genes act in parallel pathways.