In the nematode Caenorhabditis elegans, the PVD sensory neuron has an elaborate dendritic arbor that enervates the majority of the worm’s body wall muscles. During standard growth conditions, PVD dendrite morphology is effected through a well-characterized spatial and temporal growth program, and many of the molecular mechanisms which regulate this process have been described. We observe that adverse environmental conditions induce morphological plasticity in the development of the PVD dendritic arbor. This altered morphology is most notable in regard to dauer diapause – the stress-resistant alternative to larval stage 3 (L3). Larvae can survive for months in the dauer stage and re-enter normal reproductive development as L4s when environmental conditions improve. There are two modes of dauer-related morphological plasticity of the PVD dendrite: first, dauer diapause induces suspension of dendrite growth; second, after recovery from dauer, PVD exhibits exuberant dendrite elaboration. Surprisingly, mutants that increase the propensity of larvae to enter dauer instead of L3, the daf-c mutants, exhibit exuberant dendrite growth without going through dauer, suggestive that it is the dauer signaling components rather than the dauer pause itself that regulates the exuberant growth phenotype. We are developing genetic tools to characterize the tissue-specificity of dauer signaling components in regulating PVD dendrite morphology, and we are identifying the cell-intrinsic dendrite outgrowth mechanisms that are alternately regulated to mediate this morphological plasticity.