Light activation of channelrhodopsin-2 in excitable cells of Caenorhabditis elegans triggers rapid behavioral responses
Precisely controlling neurons or muscle required invasive stimulation. A gain-of-function channelrhodopsin-2 in C. elegans muscle and touch neurons was triggered by blue light. Light contracted muscle to 87% of body length in 500 ms and restored withdrawal in mec-10 mutants.
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Key findings
- Nagel et al. expressed ChR2(gf)::YFP in C. elegans body wall muscles via the myo-3 promoter and illuminated transgenic animals with blue light (450–490 nm). Muscles contracted simultaneously, reducing body length to ~87% within 500–600 ms and sustaining contraction throughout illumination. Relaxation occurred within ~1 s after light offset; controls lacking all-trans retinal showed no response.
- ChR2 expressed in mechanosensory neurons of C. elegans triggered withdrawal behaviors upon blue light illumination that mirrored responses to mechanical touch. Light-evoked behavior was absent in animals lacking retinal. In mec-4/mec-10 mutants unable to respond to touch, ChR2 expression restored light-driven withdrawal, demonstrating functional bypass of the native mechanosensory ion channel.
- ChR2-mediated muscle contractions were reduced by 62% in unc-68 ryanodine receptor mutants (p < 0.00004) and by 19% in egl-19 L-type voltage-gated Ca2+ channel reduction-of-function mutants, while unc-2 P/Q-type VGCC mutants were unaffected. These results identified ryanodine receptor-mediated Ca2+-induced Ca2+ release as the dominant pathway for ChR2-triggered muscle contraction.