title: Cell-cycle-dependent regulation of oxidative stress responses and Ca2+ permeable channels NtTPC1A/B in tobacco BY-2 cells.
abstract: Plants are always exposed to the menace of oxidative stress and protect themselves by activating a variety of defense responses. However, molecular mechanisms for oxidative stress-induced gene expression are largely unknown. We here studied the roles of the oxidative stress-responsive putative voltage-dependent Ca(2+) permeable channels, NtTPC1A and NtTPC1B, and cell cycle in H(2)O(2)-induced expression of antioxidant enzymes, glutathione peroxidase (GPX) and ascorbate peroxidase (APX), in tobacco BY-2 cells. H(2)O(2)-induced [Ca(2+)](cyt) rise and expression of GPX and APX were inhibited by the cosuppression of NtTPC1A/B as well as Al ion, a specific blocker for NtTPC1s, and enhanced by overexpression of AtTPC1, suggesting that NtTPC1s are the major Ca(2+)-permeable channels activated by H(2)O(2) and that Ca(2+) influx via NtTPC1s is involved in induction of H(2)O(2)-triggered gene expression. Oxidative stress-induced signal transduction mechanisms were highly dependent on the phases of the cell cycle; H(2)O(2)-induced [Ca(2+)](cyt) rise and expression of GPX and APX as well as the level of NtTPC1s transcripts correlated with each other and were maximal at G1 phase. In contrast, the cell cycle-dependence of hypoosmotic shock-induced [Ca(2+)](cyt) rise that is known to be independent of NtTPC1s was almost reverse and maximal at S phase. These results suggest that the cell cycle-dependent regulation of oxidative stress-induced [Ca(2+)](cyt) rise and expression of NtTPC1s contribute to the cell cycle dependence of H(2)O(2)-induced expression of peroxidases. Various Ca(2+)-mediated signal transduction pathways are differentially regulated by the cell cycle.
authors.affiliation: Department of Applied Biological Science, Tokyo University of Science, Noda, Chiba, Japan.
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Kadota
authors.forename: Takuya
authors.initials: T
authors.lastname: Furuichi
authors.forename: Toshio
authors.initials: T
authors.lastname: Sano
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Kaya
authors.forename: Wataru
authors.initials: W
authors.lastname: Gunji
authors.forename: Yasufumi
authors.initials: Y
authors.lastname: Murakami
authors.forename: Shoshi
authors.initials: S
authors.lastname: Muto
authors.forename: Seiichiro
authors.initials: S
authors.lastname: Hasezawa
authors.forename: Kazuyuki
authors.initials: K
authors.lastname: Kuchitsu
mesh_terms: D029681:Arabidopsis Proteins / Q000096:biosynthesis / Q000235:genetics; D060387:Ascorbate Peroxidases; D015220:Calcium Channels / Q000096:biosynthesis* / Q000235:genetics; D020013:Calcium Signaling / Q000502:physiology; D002453:Cell Cycle / Q000502:physiology*; D002460:Cell Line; D018506:Gene Expression Regulation, Plant; D005979:Glutathione Peroxidase / Q000096:biosynthesis; D006861:Hydrogen Peroxide / Q000494:pharmacology; D015640:Ion Channel Gating / Q000502:physiology; D018384:Oxidative Stress / Q000502:physiology*; D010544:Peroxidases / Q000096:biosynthesis / Q000378:metabolism; D010940:Plant Proteins / Q000096:biosynthesis* / Q000235:genetics; D014026:Nicotiana / Q000166:cytology / Q000378:metabolism*; D000097903:Two-Pore Channels
chemical_list: D029681:Arabidopsis Proteins; D060387:Ascorbate Peroxidases; D015220:Calcium Channels; D005979:Glutathione Peroxidase; D006861:Hydrogen Peroxide; D010544:Peroxidases; D010940:Plant Proteins; C498240:TPC1 protein, Arabidopsis; D000097903:Two-Pore Channels