can adapt and survive in dynamically changing environments by the smart and delicate switching of molecular plasticity. dauer diapause is a form of phenotypic and developmental plasticity that induces reversible developmental arrest upon environmental cues. An ER (endoplasmic reticulum)-resident Ca 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 , CALU-1 is known to function in Ca-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 () 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 mutant. Surprisingly, the dauer ratio of the () mutant was extremely low compared to that of the wild type. In fact, the () mutants were mostly unable to enter diapause. We also found that 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 .
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10044922 | PMC |
http://dx.doi.org/10.3390/biology12030464 | DOI Listing |
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