Journal
NATURE
Volume 422, Issue 6930, Pages 442-446Publisher
NATURE PORTFOLIO
DOI: 10.1038/nature01485
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Funding
- Biotechnology and Biological Sciences Research Council [BBS/E/J/00000168] Funding Source: Medline
- Biotechnology and Biological Sciences Research Council [BBS/E/J/00000168] Funding Source: researchfish
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Cell expansion is a central process in plant morphogenesis, and the elongation of roots and root hairs is essential for uptake of minerals and water from the soil. Ca2+ influx from the extracellular store is required for ( and sets the rates of) cell elongation in roots(1). Arabidopsis thaliana rhd2 mutants are defective in Ca2+ uptake and consequently cell expansion is compromised rhd2 mutants have short root hairs(2,3) and stunted roots. To determine the regulation of Ca2+ acquisition in growing root cells we show here that RHD2 is an NADPH oxidase, a protein that transfers electrons from NADPH to an electron acceptor leading to the formation of reactive oxygen species (ROS). We show that ROS accumulate in growing wild-type (WT) root hairs but their levels are markedly decreased in rhd2 mutants. Blocking the activity of the NADPH oxidase with diphenylene iodonium (DPI) inhibits ROS formation and phenocopies Rhd2(-). Treatment of rhd2 roots with ROS partly suppresses the mutant phenotype and stimulates the activity of plasma membrane hyperpolarization-activated Ca2+ channels, the predominant root Ca2+ acquisition system. This indicates that NADPH oxidases control development by making ROS that regulate plant cell expansion through the activation of Ca2+ channels.
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