PLASTID ENVELOPE ION CHANNELS (PEC1/2) link Ca 2+ and jasmonic acid signaling in plant cells.
Plants constantly encounter adverse environmental interactions. One organelle is particularly specialized in stress signaling and phytohormone synthesis: the plastid. Calcium (Ca 2+ ), a key second messenger, is known to intersect with cellular phytohormone signaling networks. While cytosolic Ca 2+ dynamics have been studied extensively, the physiological relevance of stromal Ca 2+ transients and the identity of channels mediating rapid Ca 2+ flux into plastids remain largely unexplored. In this
Plants constantly encounter adverse environmental interactions. One organelle is particularly specialized in stress signaling and phytohormone synthesis: the plastid. Calcium (Ca 2+ ), a key second messenger, is known to intersect with cellular phytohormone signaling networks. While cytosolic Ca 2+ dynamics have been studied extensively, the physiological relevance of stromal Ca 2+ transients and the identity of channels mediating rapid Ca 2+ 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 Ca 2+ 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 Ca 2+ signaling with JA-dependent stress responses and position PECs as modulators of plant defense.
