title: High REDOX RESPONSIVE TRANSCRIPTION FACTOR1 Levels Result in Accumulation of Reactive Oxygen Species in Arabidopsis thaliana Shoots and Roots.
abstract: Redox Responsive Transcription Factor1 (RRTF1) in Arabidopsis is rapidly and transiently upregulated by H2O2, as well as biotic- and abiotic-induced redox signals. RRTF1 is highly conserved in angiosperms, but its physiological role remains elusive. Here we show that inactivation of RRTF1 restricts and overexpression promotes reactive oxygen species (ROS) accumulation in response to stress. Transgenic lines overexpressing RRTF1 are impaired in root and shoot development, light sensitive, and susceptible to Alternaria brassicae infection. These symptoms are diminished by the beneficial root endophyte Piriformospora indica, which reduces ROS accumulation locally in roots and systemically in shoots, and by antioxidants and ROS inhibitors that scavenge ROS. More than 800 genes were detected in mature leaves and seedlings of transgenic lines overexpressing RRTF1; ∼ 40% of them have stress-, redox-, ROS-regulated-, ROS-scavenging-, defense-, cell death- and senescence-related functions. Bioinformatic analyses and in vitro DNA binding assays demonstrate that RRTF1 binds to GCC-box-like sequences in the promoter of RRTF1-responsive genes. Upregulation of RRTF1 by stress stimuli and H2O2 requires WRKY18/40/60. RRTF1 is co-regulated with the phylogenetically related RAP2.6, which contains a GCC-box-like sequence in its promoter, but transgenic lines overexpressing RAP2.6 do not accumulate higher ROS levels. RRTF1 also stimulates systemic ROS accumulation in distal non-stressed leaves. We conclude that the elevated levels of the highly conserved RRTF1 induce ROS accumulation in response to ROS and ROS-producing abiotic and biotic stress signals.
authors.affiliation: Institute of Plant Physiology, Friedrich-Schiller University Jena, Dornburger Straße 159, 07743 Jena, Germany; Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, 1-5 Hangi-cho, Shimogamo, Sakyo-ku, Kyoto 606-8522, Japan.
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Matsuo
authors.affiliation: Institute of Plant Physiology, Friedrich-Schiller University Jena, Dornburger Straße 159, 07743 Jena, Germany.
authors.forename: Joy Michal
authors.initials: JM
authors.lastname: Johnson
authors.affiliation: Faculty of Applied Biological Sciences, Gifu University, Yanagido 1-1, Gifu City 501-1193, Japan.
authors.forename: Ayaka
authors.initials: A
authors.lastname: Hieno
authors.affiliation: Faculty of Applied Biological Sciences, Gifu University, Yanagido 1-1, Gifu City 501-1193, Japan.
authors.forename: Mutsutomo
authors.initials: M
authors.lastname: Tokizawa
authors.affiliation: Center for Gene Research, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan.
authors.forename: Mika
authors.initials: M
authors.lastname: Nomoto
authors.affiliation: Center for Gene Research, Nagoya University, Furo-cho, Chikusa-ku, Nagoya 464-8601, Japan.
authors.forename: Yasuomi
authors.initials: Y
authors.lastname: Tada
authors.affiliation: Institute of Molecular Cell Biology, Center for Molecular Biomedicine, Jena University Hospital, 00743 Jena, Germany; Molecular Cardiology, Department of Cardiovascular Medicine, University Hospital Münster, 48149 Münster, Germany.
authors.forename: Rinesh
authors.initials: R
authors.lastname: Godfrey
authors.affiliation: Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, 1-5 Hangi-cho, Shimogamo, Sakyo-ku, Kyoto 606-8522, Japan.
authors.forename: Junichi
authors.initials: J
authors.lastname: Obokata
authors.affiliation: Institute of Plant Physiology, Friedrich-Schiller University Jena, Dornburger Straße 159, 07743 Jena, Germany.
authors.forename: Irena
authors.initials: I
authors.lastname: Sherameti
authors.affiliation: Faculty of Applied Biological Sciences, Gifu University, Yanagido 1-1, Gifu City 501-1193, Japan.
authors.forename: Yoshiharu Y
authors.initials: YY
authors.lastname: Yamamoto
authors.affiliation: Institute of Molecular Cell Biology, Center for Molecular Biomedicine, Jena University Hospital, 00743 Jena, Germany.
authors.forename: Frank-D
authors.initials: FD
authors.lastname: Böhmer
authors.affiliation: Institute of Plant Physiology, Friedrich-Schiller University Jena, Dornburger Straße 159, 07743 Jena, Germany. Electronic address: b7oera@hotmail.de.
authors.forename: Ralf
authors.initials: R
authors.lastname: Oelmüller
mesh_terms: D000111:Acetylcysteine / Q000494:pharmacology; D000528:Alternaria / Q000502:physiology; D017360:Arabidopsis / Q000378:metabolism* / Q000382:microbiology; D029681:Arabidopsis Proteins / Q000235:genetics / Q000378:metabolism*; D001483:Base Sequence; D016923:Cell Death / Q000187:drug effects; D004050:Ditiocarb / Q000494:pharmacology; D018506:Gene Expression Regulation, Plant / Q000187:drug effects; D017343:Genes, Plant; D008027:Light; D008969:Molecular Sequence Data; D000069452:Pathogen-Associated Molecular Pattern Molecules / Q000378:metabolism; D010641:Phenotype; D010935:Plant Diseases / Q000235:genetics / Q000382:microbiology; D018517:Plant Roots / Q000187:drug effects / Q000235:genetics / Q000378:metabolism* / Q000528:radiation effects; D018520:Plant Shoots / Q000187:drug effects / Q000378:metabolism* / Q000528:radiation effects; D030821:Plants, Genetically Modified; D011401:Promoter Regions, Genetic / Q000235:genetics; D017382:Reactive Oxygen Species / Q000378:metabolism*; D036226:Seedlings / Q000187:drug effects / Q000235:genetics / Q000382:microbiology / Q000528:radiation effects; D013312:Stress, Physiological / Q000187:drug effects / Q000235:genetics / Q000528:radiation effects; D014157:Transcription Factors / Q000235:genetics / Q000378:metabolism*
chemical_list: D029681:Arabidopsis Proteins; D000069452:Pathogen-Associated Molecular Pattern Molecules; C535225:RRTF1 protein, Arabidopsis; D017382:Reactive Oxygen Species; D014157:Transcription Factors; D004050:Ditiocarb; D000111:Acetylcysteine
keywords: H(2)O(2); RAP2.6; REDOX RESPONSIVE TRANSCRIPTION FACTOR1; RRTF1 promoter binding sites; abiotic and biotic stress; reactive oxygen species