PLASTID ENVELOPE ION CHANNELS (PEC1/2) link Ca2+ and jasmonic acid signaling in plant cells

• 成果类型: Article
• 署名作者: Muhlbauer, Susanne; Jaslan, Dawid; Duarte Nunes, Ines F.; Brandt, Benjamin; Wutz, Lena; Mekkaoui, Khansa; Zenker, Sanja; Rehberger, Jakob; Radler, Marlena; Holzner, Lorenz; Tisserant, Constance; Volkner, Carsten; Brautigam, Andrea; Robatzek, Silke; Hause, Bettina; Grimm, Christian; Kunz, Hans-Henning
• 署名单位: University of Munich; Leibniz Institut fur Pflanzenbiochemie; University of Bielefeld; University of Bielefeld; University of Munich; University of Oxford
• 刊物名称: PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
• ISSN/ISSBN: 0027-8424; 1091-6490
• DOI: 10.1073/pnas.2525536123
• 发表日期: 2026-09-01
• 页码: e2525536123
• 关键词: CHLOROPLAST; ion channels; JASMONIC ACID; stress defense; Ca2+ signaling; gene-expression; arabidopsis; DEFENSE; GROWTH; activation; binding; stress; allele; shape

摘要

Plants constantly encounter adverse environmental interactions. One organelle is particularly specialized in stress signaling and phytohormone synthesis: the plastid. Calcium (Ca2+), a key second messenger, is known to intersect with cellular phytohormone signaling networks. While cytosolic Ca2+ dynamics have been studied extensively, the physiological relevance of stromal Ca2+ transients and the identity of channels mediating rapid Ca2+ flux into plastids remain largely unexplored. In this study, we provide evidence for PLASTID ENVELOPE ION CHANNELS (PECs) as long-sought mediators of fast-activating cation channel-like currents. We show that PEC expression is jasmonic acid (JA)-induced to augment stromal Ca2+ transients under stress. Loss of PECs results in decreased JA priming and failure to elicit full defense responses after wounding. In turn, PEC1 overexpression improves Botrytis cinerea tolerance. Our findings link stromal Ca2+ signaling with JA-dependent stress responses and position PECs as modulators of plant defense.