Individual welfare depends on maintenance of homeostasis. Long-lasting adverse environments results in stressful conditions that may damage the organism. We have shown in mammal models that chronic stress paradigms -which resemble human depressive states- alter brain GPM6A levels. The GPM6A participates in neuronal differentiation and morphology establishment. There is a gap between the cellular GPM6A functions and its role in systemic stress response. The nematode C. elegans exhibits a GPM6A ortholog, the neuronal membrane glycoprotein 1 (NMGP-1). Due to shared features between nematode and mammals and because of the genetic tools available, we used C. elegans as a simpler model to study NMGP-1 participation in stress response. We have characterized NMGP-1 functions using RNAi knockdown and two non-null, hypomorphic mutant alleles. Analysis of interfered or mutant alleles showed a reduced egg-laying rate and an increased recovering time from the stress-resistant dauer stage. In addition, defects in egg-laying induced egg retention in nmgp-1-deficient worms. In addition, worms lacking NMGP-1 showed a normal response to attractant such as diacetyl, but an altered repulsive response to SDS. Moreover, nmgp-1(RNAi) worms showed morphological alterations on ASJ chemosensory neurons, responsible of dauer exit. Altogether these results shed light in NMGP-1 role in C. elegans. These mutants represent an attractive platform to test drugs modulating stress response.