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Figure 1 | Molecular Brain

Figure 1

From: Identification of key structural elements for neuronal calcium sensor-1 function in the regulation of the temperature-dependency of locomotion in C. elegans

Figure 1

Loss of function of ncs-1 prevents acute inhibition of locomotion following temperature elevation in a temperature-dependent locomotion (TDL) assay. (A). Locomotion rates of wild-type Bristol N2 and ncs-1 null (qa406) worms were quantified at room temperature (20°C; open bars) and then after elevation of temperature to 28°C for 10 min (filled bars). N2 worms showed a substantial reduction in locomotion at elevated temperature (*; P < 0.01) but in contrast the ncs-1 null worms showed an increase rate of locomotion at 28°C (*; P < 0.01, n = 100 worms for each condition). (B) Transgenic expression of NCS-1 rescued the TDL assay phenotype. The locomotion at 20°C and 28°C of three separate lines of transgenic worms expressing NCS-1 under the control of its endogenous promoter (res 1–3) was compared to that of N2 wild-type and ncs-1 null worms (n = 7-12 for each worm line). (C) Non-myristoylatable NCS-1 was able to rescue function in the TDL assay. The locomotion at 20°C and 28°C of three separate lines of transgenic worms expressing NCS-1 (G2A) in the ncs-1 null background was compared to that of N2 wild-type and ncs-1 null worms. The data from separate worm lines was pooled and the data normalised to the locomotion rate of N2 worms at 20°C and the rate of movement at 20°C and 28°C compared for each condition (*; P < 0.01, n = 10 for N2 and qa406, n = 30 for G2A). Statistical significance was determined using the Mann–Whitney U test with use of the Bonferonni correction for multiple comparisons.

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