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Ion-channel blocker sensitivity of voltage-gated calcium-channel homologue Cch1 in Saccharomyces cerevisiae

Jinfeng Teng^1,2,

Rika Goto^1,

¹ Department of Biology, Tokyo Gakugei University, 4-1-1 Nukui kita-machi, Koganei-shi, Tokyo 184-8501, Japan
² Laboratory of Cell Biology, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Gunma 371-8510, Japan
³ Biomembrane Signaling Project 2, Tokyo Metropolitan Institute of Medical Science, 3-18-22 Honkomagome, Bunkyo-ku, Tokyo 113-8613, Japan
⁴ Department of Bioenvironmental Science, Okazaki Institute for Integrative Bioscience, National Institutes of Natural Sciences, Higashiyama 5-1, Myodaiji, Okazaki, Aichi 444-8787, Japan

Correspondence
Hidetoshi Iida
iida{at}u-gakugei.ac.jp

The Cch1 protein of the yeast Saccharomyces cerevisiae is a homologue of the pore-forming ₁ subunit of mammalian voltage-gated Ca²⁺ channels (VGCCs), and it constitutes a high-affinity Ca²⁺-influx system with the Mid1 protein in this organism. Here, we characterized the kinetic property of a putative Cch1–Mid1 Ca²⁺ channel overexpressed in S. cerevisiae cells, and showed that the L-type VGCC blockers nifedipine and verapamil partially inhibited Cch1–Mid1 activity, but typical P/Q-, N-, R- and T-type VGCC blockers did not inhibit activity. In contrast, a third L-type VGCC blocker, diltiazem, increased Cch1–Mid1 activity. Diltiazem did not increase Ca²⁺ uptake in the cch1 and mid1 single mutants and the cch1 mid1 double mutant, indicating that the diltiazem-induced increase in Ca²⁺ uptake is completely dependent on Cch1–Mid1. These results suggest that Cch1 is pharmacologically similar to L-type VGCCs, but the interactions between Cch1 and the L-type VGCC blockers are more complicated than expected.

These authors contributed equally to this work.