LAUSR

Simple Summary C. elegans dauer is a form of phenotypic and developmental plasticity that induces reversible developmental arrest upon adverse environmental cues. This is well conserved among nematodes, including in human-infective species that cause filariasis, which is a major neglected tropical disease with considerable morbidity throughout tropical countries. The infective larval stage of parasitic nematodes is equivalent to the dauer stage of free-living nematodes; thus, it is important to elucidate the unknown molecular mechanisms behind dauer development. In this sense, to understand the infective mechanism of human-infective nematodes, it is worthwhile to study the novel function of calumenin in C. elegans dauer formation. In this study, we first found that calumenin is strongly expressed in body-wall muscle and AIA interneurons at the dauer stage. In addition, the functional loss of calumenin led to failures in dauer formation induced by either single pheromone compounds or crude pheromone extracts, which are generally used to induce dauer formation in C. elegans. Based on the transcriptional and translational expression of calumenin at the dauer stage, our results suggest that calumenin may function in signaling pathways that regulate dauer formation by a yet unknown mechanism. Abstract Caenorhabditis elegans can adapt and survive in dynamically changing environments by the smart and delicate switching of molecular plasticity. C. elegans dauer diapause is a form of phenotypic and developmental plasticity that induces reversible developmental arrest upon environmental cues. An ER (endoplasmic reticulum)-resident Ca2+ binding protein, calumenin has been reported to function in a variety of malignant diseases in vertebrates and in the process of muscle contraction–relaxation. In C. elegans, CALU-1 is known to function in Ca2+-regulated behaviors (pharyngeal pumping and defecation) and cuticle formation. The cuticles of dauer larvae are morphologically distinct from those of larvae that develop in favorable conditions. The structure of the dauer cuticle is thicker and more highly reinforced than that of other larval stages to protect dauer larvae from various environmental insults. Since the calu-1(tm1783) mutant exhibited abnormal cuticle structures such as highly deformed annuli and alae, we investigated whether CALU-1 is involved in dauer formation or not. Ascaroside pheromone (ascr#2) and crude daumone were used under starvation conditions to analyze the rate of dauer formation in the calu-1(tm1783) mutant. Surprisingly, the dauer ratio of the calu-1(tm1783) mutant was extremely low compared to that of the wild type. In fact, the calu-1(tm1783) mutants were mostly unable to enter diapause. We also found that calu-1 is expressed in body-wall muscle and AIA interneurons at the dauer stage. Taken together, our results suggest that CALU-1 is required for normal entry into diapause in C. elegans.