Abstract
ABSTRACTPungent substances, such as capsaicin and gingerol, activate the transient receptor potential (TRP)-V1 channel and affect the feeding behaviors of animals. To gain insight into how living organisms have acquired a sense for pungent substances, we explored the response to TRP agonists in a protist, Chlamydomonas reinhardtii. When capsaicin or gingerol was applied to wild-type cells, they became immotile, with flagella detaching from the cell body. The degree of deflagellation was nearly halved in a mutant defective in the TRP channel ADF1. Deflagellation in the adf1 mutant was inhibited further by Ruthenium Red, indicating ADF1 and another TRP channel are involved in the deflagellation response. The response to capsaicin and gingerol was not inhibited by TRPV1-specific blockers such as 4-(3-Chloro-2-pyridinyl)-N-[4-(1,1-dimethylethyl)phenyl]-1-piperazinecarboxamide (BCTC) and capsazepine. When capsaicin or gingerol was applied to wild-type cells in the presence of Ruthenium Red, a large proportion lost motility while flagella remained attached, suggesting that flagella stop contributing to motility, at least in part, through a TRP-channel-independent pathway. These results indicate that pungent compounds such as capsaicin and gingerol induce loss of flagellar motility and flagellar detachment in C. reinhardtii cells.
Highlights
Living organisms have various sensors to detect environmental and bodily conditions
Observation at higher magnification revealed that flagella were detached from the cell body, indicating that the loss of motility was due to deflagellation
Applying 200 μM capsaicin decreased the proportion of motile cells (%motility) to less than 10% and increased the proportion of deflagellated cells (%deflagellation) to 90% (Fig. 1D,E)
Summary
Living organisms have various sensors to detect environmental and bodily conditions. In animals, ion channels called transient receptor potential (TRP) channels respond to chemical, thermal and mechanical stimuli. Detach from the cell body on application of capsaicin or gingerol, and that the ADF1 channel is involved in the deflagellation response. Channel antagonists When capsaicin was applied at various concentrations, less than half of cells responded at 50 μM and more than half at 100 μM in terms of motility loss and deflagellation, indicating an EC50 for capsaicin is between 50–100 μM (Fig. 2A).
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