한빛사 논문
Hye-In Nam1, Zaigham Shahzad2, Yanniv Dorone1,3, Sophie Clowez1, Kangmei Zhao1, Nadia Bouain3, Katerina S. Lay-Pruitt4,5, Huikyong Cho3, Seung Y. Rhee1,* & Hatem Rouached4,5,6,*
1Department of Plant Biology, Carnegie Institution for Science, Stanford, CA, USA. 2Department of Cell and Developmental Biology, John Innes Centre, Norwich NR4 7UH, UK. 3Department of Biology, Stanford University, Stanford, CA 94305, USA. 4Plant Resilience Institute, Michigan State University, East Lansing, MI 48824, USA. 5Department of Plant, Soil, and Microbial Sciences, Michigan State University, East Lansing, MI 48824, USA. 6BPMP, Univ Montpellier, CNRS, INRAE, Montpellier SupAgro, Montpellier, France.
*Corresponding author.
Abstract
Iron deficiency hampers photosynthesis and is associated with chlorosis. We recently showed that iron deficiency-induced chlorosis depends on phosphorus availability. How plants integrate these cues to control chlorophyll accumulation is unknown. Here, we show that iron limitation downregulates photosynthesis genes in a phosphorus-dependent manner. Using transcriptomics and genome-wide association analysis, we identify two genes, PHT4;4 encoding a chloroplastic ascorbate transporter and bZIP58, encoding a nuclear transcription factor, which prevent the downregulation of photosynthesis genes leading to the stay-green phenotype under iron-phosphorus deficiency. Joint limitation of these nutrients induces ascorbate accumulation by activating expression of an ascorbate biosynthesis gene, VTC4, which requires bZIP58. Furthermore, we demonstrate that chloroplastic ascorbate transport prevents the downregulation of photosynthesis genes under iron-phosphorus combined deficiency through modulation of ROS homeostasis. Our study uncovers a ROS-mediated chloroplastic retrograde signaling pathway to adapt photosynthesis to nutrient availability.
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