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.
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 pathway. 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 systems.). 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.