As a sensory response to starvation or overcrowding, Caenorhabditis elegans second-stage larvae may molt into a developmentally arrested state called the dauer larva. When environmental conditions become favorable for growth, dauer larvae mold and resume development. Some mutants unable to form dauer larvae are simultaneously affected in a number of sensory functions, including chemotaxis and mating. The behavior and sensory neuroanatomy of three such mutants, representing three distinct genetic loci, have been determined and compared with wild-type strain. Morphological abnormalities in afferent nerve endings were detected in each mutant. Both amphid and outer labial sensilla are affected in the mutant CB1377 (daf-6)X, while another mutant, CB1387 (daf-10)IV, is abnormal in amphidial cells and in the tips of the cephalic neurons. The most pleitropic mutant, CB1379 (che-3)I, exhibits gross abnormalities in the tips of virtually all anterior and posterior sensory neurons. The primary structural defect in CB1377 appears to be in the nonneuronal amphidial sheath cells. The disruption of neural organization in CB1377 is much greater in the adult than in the L2 stage. Of all the anterior sense organs examined, only the amphids are morphologically affected in all three mutants. Thus, one or more of the amphidial neurons may mediate the sensory signals for entry into the dauer larva stage in normal animals. Using temperature-sensitive mutants we determined that the same defects which block entry into the dauer stage also prevent recovery of dauer larvae.