Cilia and flagella can alter their beating patterns through changes in membrane excitation mediated by Ca(2+) influx [1-6]. The ion channel that generates this Ca(2+) influx and its cellular distribution have not been identified. In this study, we analyzed the Chlamydomonas ppr2 mutant, which is deficient in the production of a flagellar Ca(2+) current and consequently has a defective photophobic response [7] and mechanoshock response. ppr2 had a mutation in CAV2, which encodes a homolog of the alpha(1) subunit of voltage-dependent calcium channels (VDCCs). CAV2 has four domains, each with six transmembrane segments and EEEE loci in the ion-selective filter, which are typical of VDCCs in vertebrates. Interestingly, we found that CAV2 primarily localized toward the distal part of flagella. We provide evidence that CAV2 is transported toward the flagellar tip via intraflagellar transport (IFT) because CAV2 accumulated near the flagellar base when IFT was blocked. The results of this study suggest that the Ca(2+) influx of Chlamydomonas flagella is mediated by the VDCC, CAV2, whose distribution is biased to the distal region of the flagellum.