Worm Breeder's Gazette 14(4): 51 (October 1, 1996)

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.

Is the dauer an alternative larval stage?

Chris Link

Institute for Behavioral Genetics, U. Colorado, Campus Box 447, Boulder, CO, 80309

  Or is it the L3?  I would like to raise the possibility that our "worm
plate perspective" of C. elegans may have biased our view of the dauer
larvae stage.  It would seem likely that dauer larvae are much more
prevalent in the dirt than on our (unstarved) plates, so which stage is
viewed as alternative probably depends on the environmental context.  I
do not believe this is just a matter of semantics, because it can
influence the way we think about the dauer pathway.  It has always
struck me as surprising that both ablation of specific neurons and
inactivation of genes involved in a presumptive TGF beta induction
pathway (e.g., daf-1, daf-4, daf-7, etc.) cause a dauer constitutive
pathway.  Perhaps it is more appropriate, therefore, to consider these
neurons and genes as part of  an L3 induction pathway.  In this view,
the inability to induce the L3 results in a default to the dauer

  While I am engaging in rampant (and recklessly unsupported)
speculation, let me also suggest the possibility that the ability to
make L3s may be a derived character in the C. elegans lineage; that is,
the C. elegans ancestor may have had an obligate dauer stage (instead of
an L3).  This may not be as farfetched as it sounds, as plant parasitic
nematodes have an obligate juvenile (non-feeding) infective stage
analogous (and homologous?) to dauer larvae.  In this view, C. elegans
has evolved (or re-evolved) the ability to induce the L3.  Admittedly,
there is probably no present phylogenetic evidence (such as the
existence of a related free-living species with obligate dauers) that
convincingly supports this possibility.  If there is some truth to this
idea, it might help explain the apparent complexity of the dauer pathway
(i.e., by the evolutionary accumulation and overlay of regulatory

  Does this view suggest any experiments?  If  the daf TGF beta pathway
is actually directly involved in L3 induction, then mis-timed expression
of these components might lead to heterochronic  effects, by
inappropriate induction of L3 development.  If  both L3 and dauer larvae
development require induction, then there should be double mutant
combinations that lead to larval arrest, because neither the L3 nor the
dauer stage can be induced.  A corollary of the "old dauer" view is that
dauer-related capacities, such as the ability to sense dauer pheromone,
may have been around for a long time.  If this is the case, one might
suspect that the ability to establish the pheromone/food ratio may be
employed at multiple developmental stages, not just for the dauer/L3
decision.  It would therefore be very interesting to examine the effect
of pheromone on L4/adult animals, particularly in respect to rate of egg
production, longevity, and the enhanced stress response that is
associated with longevity-increasing mutations in genes such as daf-2
and daf-23.