Worm Breeder's Gazette 12(2): 85 (January 1, 1992)

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.

The Ethics of Dauer Formation: Two Wrongs Make a Right?

Jennifer Vowels, Jim Thomas

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Department of Genetics, University of Washington, Seattle, WA.

Dauer larva formation in C. elegans requires chemosensation of a dauer pheromone. Mutations in genes required for the dauer pheromone response cause either a dauer defective (Daf-d) or a dauer constitutive (Daf-c) phenotype. By epistasis analysis, these genes have been ordered into a negative regulatory pathway of gene action (Vowels and Thomas, 1992; Riddle, et al., 1981). In double mutants between the Daf-c gene, daf-11 ,and a set of dauer defective mutants with structurally abnormal chemosensory cilia (e.g. osm-1 , osm-3 , che-11 , che-13 , daf-6 and daf-10 ,Perkins, et al., 1986, Albert, et al, 1981), the Daf-c phenotype of daf-11 is suppressed (see Table 1 and Vowels and Thomas, 1992). These results suggest that daf-11 is acting upstream of this class of chemosensory cilium mutants, and requires wild type chemosensory cilia for proper signal transduction. Therefore, daf-11 is a good candidate for one of the proximal signal transduction components in the pheromone sensing pathway.

The unc-104 gene encodes a protein with homology to heavy chain kinesins, and appears to be involved in organelle transport (Otsuka, et al., 1991; Hall and Hedgecock, 1991). We have found that the partial loss-of-function unc-104 ( e1265 )mutant responds more weakly to dauer pheromone than the wild type, and makes fewer dauers than normal on starved plates. To test for possible interactions among unc-104 , daf-11 ,and the cilium structure mutants osm-1 and osm-3 ,we constructed several double and triple mutant strains and tested for constitutive dauer formation at 25°C (Table 1).

[See Figure 1]

Two surprising results were observed. First, although an osm-1 ( p808 )mutant is dauer defective, and an unc-104 ( e1265 )mutant is partially dauer defective, the double mutant between them is dauer constitutive. Double mutants between unc-104 ( e1265 )and other alleles of osm-1 give similar results. In addition, we have constructed double mutants between unc-104 ( e1265 )and other mutations that affect amphid structure; the che-13 ( e1124 )and che-11 ( e1810 )double mutants show a low level of dauer constitutivity (<15%), while the daf-6 ( e1377 )and daf-10 ( e1387 )double mutants show no dauer constitutivity. Finally, this result is not dependent on the unc-104 allele used, as unc-104 ( rh1017 ); osm-1 ( p808 )double mutants are slightly dauer constitutive. A formal interpretation of these results is that unc-104 and osm-1 encode functionally redundant proteins that are required to repress dauer formation in the absence of inducing conditions.

The second surprising result is that although daf-11 with osm-3 or osm-1 makes almost no dauers, and unc-104 also makes no dauers under non-inducing conditions, the daf-11 ; unc-104 triple mutants with osm-3 and osm-1 are strongly dauer constitutive. This result suggests that in the absence of unc-104 function, the daf-11 mutant phenotype no longer requires wild type sensory cilia.

Literature Cited:


1. Albert, P., et al. (1981) J. of Comp. Neurology 198: 435-451.

2. Hall and Hedgecock (1991) Cell 65: 837-847.

3. Otsuka, A., et al. (1991) Neuron 6: 113-122.

4. Perkins, L., et al. (1986) Dev. Bio. 117: 456-487.

5. Riddle, D., et al. (1981) Nature 290: 668-671.

6. Vowels and Thomas (1992) Genetics, in press.

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