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Fig. 1 | BMC Biology

Fig. 1

From: Genetic modifiers ameliorate endocytic and neuromuscular defects in a model of spinal muscular atrophy

Fig. 1

Rescue of smn-1(cb131) exhaustion defects by reintroduction of smn-1(+). a Schematic representation of experimental design. Channelrhodopsin is expressed in cholinergic motor neurons. After overnight retinal feeding, animals are exposed to blue light stimuli for 20 s in liquid and body bends per minute are recorded over time. A body bend is defined as a muscle contraction resulting in a dorsal to ventral movement across the midline of the animal. b Before blue light stimulation, animals have almost identical locomotion (data points shown in gray). After 20 s blue light stimulation of channelrhodopsin (ChR2) in cholinergic neurons, smn-1(cb131) partial loss of function animals had decreased locomotion rates when fed retinal and had delayed recovery to original activity. Animals not fed retinal are shown immediately following blue light exposure in a hashed box. Locomotion reported as body bends per minute in liquid. c Introduction of an smn-1 genomic transgene restored normal locomotion rates immediately following blue light illumination. [smn-1(+)] is rtSi10, a homozygous single-copy insertion on chromosome IV (see Additional file 1: Table for details); ANOVA F(3.32, 12.5) = 7.27, p < 0.05. All animals carry oxIs364[unc-17p::ChR2] and exhibit no change in locomotion without exogenous retinal feeding (data not shown). The drop in body bends per minute from panel b to c is due to methodology. Panel b is counted manually by eye whereas panel c and future locomotion rates are calculated using the NABAS program described in the “Methods” section. For all locomotion assays, n ≥ 30 animals were used per determination and combined from 3 independent and blinded trials. Student’s t test: *p < 0.05, **p < 0.01. SEM indicated

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