Worm Breeder's Gazette 11(1): 52

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.

Dauer Larva Formation in unc-31 Animals

Cori Bargmann and Bob Horvitz

Figure 1

Dauer larva formation is regulated by the presence of food and dauer 
pheromone in the worm's environment.  Wild-type C.  elegans animals 
become dauer larvae inappropriately (in the presence of bacteria) if 
four sensory cell types, the amphid cells ADF, ASG, ASI, and ASJ, are 
killed with a laser microbeam (WBG 10: 2, p.42).  We infer that these 
sensory cells recognize either food, pheromone, or both stimuli.  Leon 
Avery has described a mutation, aex-3(ad418) X, that has a synthetic 
dauer constitutive phenotype in combination with unc-311e928) IV ,WBG 
10: 2, p.39).  aex-3 also has a pharyngeal pumping defect in 
combination with unc-31; de 
redundant functions in these two processes.  We thought the redundancy 
between these two genetic functions might correspond to the redundancy 
among sensory neurons controlling dauer formation.  To test this idea, 
we killed sensory neurons in unc-31 animals and observed the 
development of the altered animals in the presence of plentiful 
bacteria.  Selected data are shown 
[See Figure 1]
Only one of the four cells that can prevent dauer formation in N2 
seems to be active in unc-31, since the death of ASI is sufficient to 
lead to dauer formation.  We conclude that ADF, ASG, and ASJ are 
functionally inactivated in unc-31 animals.  This could be due to a 
requirement for the unc-31 gene product either in the sensory cells or 
in cells that act as their targets in dauer formation.
The suggestion that unc-31 is required for sensory neuron function 
is supported by our observation that unc-31 animals are unable to 
chemotax to aqueous (Cl-, cAMP) or volatile (benzaldehyde, isoamyl 
alcohol) attractants.  Since killing ADF, ASG, and ASJ does not lead 
to chemotaxis defects of that severity, it seems likely that 
additional cells are affected by unc-31 mutations.
Alberts and Riddle (J.  Comp.  Neurol.  219:461 (1983)) have 
described a remodeling of the amphid sensilla in dauer larvae.  As a 
result of this remodeling, the sensory neurons ASG and ASI are not 
exposed to the environment in dauer larvae, although they are in 
normal larvae and adults.  This could render those neurons insensitive 
to external stimuli in dauer larvae and therefore unable to mediate 
recovery from the dauer stage.  Indeed, we have found through laser 
experiments that only ASJ and possibly ADF appear to affect recovery 
of wild-type animals from the dauer stage.
By the above arguments, if ASI is the only sensory neuron that 
regulates dauer formation in unc-31 animals, those animals ought to be 
unable to recover from the dauer stage.  We generated unc-31 dauer 
larvae by starvation and crowding, and examined their ability to 
recover and form adults after adding bacteria.  50/50 wildtype animals 
recovered from the dauer stage at 20 C in 24 hours, but only 5/122 unc-
31 animals recovered under the same conditions in a two week period.  
Thus unc-31 animals are extremely defective in recovery from the dauer 
unc-31 animals will recover from the dauer stage when shifted to 15 
C, but only slowly - half the dauers recovered in 5 days at 15 C.  The 
recovery at 15 C might be caused by temperature-sensitivity of e928, 
or it might reflect the intrinsic temperature sensitivity of dauer 
formation noted in the study of other mutants.

Figure 1