Methods for Modulating and Measuring Neuromuscular Exertion in C. elegans.

The nematode C. elegans has been used widely to study the genetic and cellular basis of behavior. Yet the laboratory conditions under which it is typically studied offer only a narrow glimpse into the richness of natural behaviors this remarkable animal evolved over 500 million years of evolution. For example, burrowing behavior naturally occurs in the wild, but it remains understudied. Our group studies burrowing in an attempt to expand our understanding of the natural behavioral repertoire of C. elegans. Aside from being an interesting and tractable behavior, burrowing is experimentally useful and permits the titration of the muscular output exerted by C. elegans. Here we describe several burrowing assays that allow the modulation of muscular exertion. We used these to study both adaptive and pathological muscular processes such as muscle hypertrophy and dystrophy, respectively. We believe these assays will be of use for researchers studying the production of locomotion under normal and disease-challenged conditions.

Neuronal membrane glycoprotein (nmgp-1) gene deficiency affects chemosensation-related behaviors, dauer exit and egg-laying in Caenorhabditis elegans.

The nervous system monitors the environment to maintain homeostasis, which can be affected by stressful conditions. Using mammalian models of chronic stress, we previously observed altered brain levels of GPM6A, a protein involved in neuronal morphology. However, GPM6A's role in systemic stress responses remains unresolved. The nematode Caenorhabditis elegans expresses a GPM6A ortholog, the neuronal membrane glycoprotein 1 (NMGP-1). Because of the shared features between nematode and mammalian nervous systems and the vast genetic tools available in C. elegans, we used the worm to elucidate the role of GPM6A in the stress response. We first identified nmgp-1 expression in different amphid and phasmid neurons. To understand the nmgp-1 role, we characterized the behavior of nmgp-1(RNAi) animals and two nmgp-1 mutant alleles. Compared to control animals, mutant and RNAi-treated worms exhibited increased recovery time from the stress-resistant dauer stage, altered SDS chemosensation and reduced egg-laying rate resulting in egg retention (bag-of-worms phenotype). Silencing of nmgp-1 expression induced morphological abnormalities in the ASJ sensory neurons, partly responsible for dauer exit. These results indicate that nmgp-1 is required for neuronal morphology and for behaviors associated with chemosensation. Finally, we propose nmgp-1 mutants as a tool to screen drugs for human nervous system pathologies.