Figure 3. dmsr-1 mutants are defective in quiescence associated with stress-induced sleep.

(A) Rate of pharyngeal pumping before and up to two hours following heat pulse induction of EGF/LIN-3C overexpression. dmsr-1 does not suppress EGF induced feeding quiescence. (B) dmsr-1(qn45) partially suppresses body movement quiescence induced by EGF overexpression (Phsp-16.2:lin-3). Body movements were measured for two hours starting one hour after induction of EGF overexpression. (C) Rate of pharyngeal pumping in dmsr-1(qn45) mutants and dmsr-1 genomic rescue during the first hour following 35°C heat shock to induce SIS. Rescue construct is the operon-based reporter shown in Figure 5. Asterisks denote significant difference compared to dmsr-1(qn45). (D) Body movement quiescence during 90 min after a 35°C heat shock. The dmsr-1(qn45) mutation suppresses body movement quiescence in response to heat shock. This defect in quiescence is rescued by a genomic fragment containing dmsr-1. Statistical significance was assessed using a 2-Way ANOVA with post-hoc pairwise comparisons made using Bonferroni correction method. Error bars denote Mean ± SEM. *p<0.05, **p<0.01, ***p<0.001.

DOI: http://dx.doi.org/10.7554/eLife.19837.006

Figure 3—figure supplement 1. dmsr-1 mutants are defective in SIS triggered by different stressors but are not defective in developmentally timed sleep during lethargus.

(A) Total body movement quiescence during the first hour after exposure to the indicated temperature for 30 min. Error bars denote SEM. ***p<0.001. (B) Total body movement quiescence each hour after exposure to ultraviolet C (UVC) light. Error bars denote SEM. ***p<0.001. (C) Total body movement quiescence in the three hours after the start of L4 lethargus. NS denotes p>0.05.In panels A and B, statistical significance was assessed 2-Way ANOVA with post-hoc pairwise comparisons made using Bonferroni correction method, and in C with a two-tailed Student’s t test.

DOI: http://dx.doi.org/10.7554/eLife.19837.007