What is it about?
Plants must react quickly when attacked by herbivores or pathogens. Two important pathways in this process are calcium signaling and the stress hormone jasmonic acid (JA). Calcium signals are elicited within seconds after stress perception and distribute information about the attack throughout the plant, while JA activates and sustains defense responses. Our study identifies PLASTID ENVELOPE ION CHANNELS (PECs) as links between these two signaling systems. PECs transmit fast cation currents into the chloroplast and mediate stress-induced calcium flux from the cytosol into chloroplasts. Intriguingly, PEC expression is induced by JA signaling, and PEC levels accumulate substantially within 12 hours to stay elevated for days. This creates a feed-forward mechanism in which stress increases PEC1 protein levels, which exacerbates stress-induced chloroplast calcium signals and ultimately supports the accumulation of JA during recurring stress to elicit a faster and stronger stress response.
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Why is it important?
Chloroplasts play key roles in the biogenesis of several plant hormones, including JA. At the same time, plastids generate rapid calcium transients in their stroma in response to various stress triggers. However, the physiological relevance of these calcium transients for plants remained poorly understood. By identifying PEC channels as regulators of chloroplast calcium signaling and JA-mediated defense, our study provides a molecular tool for fine-tuning plant defense. Plants lacking PECs show impaired JA accumulation under recurring stress and are more susceptible to the fungus Botrytis cinerea, while PEC1 overexpressors exhibit stronger JA-dependent defense priming and enhanced resistance. Importantly, PECs do not act as simple on/off switches. Instead, they finely tune where calcium signals go inside plant cells and thereby help shape JA-dependent defense during repeated stress while leaving baseline hormonal defense unchanged. This may explain why PEC1 overexpressors show only mild growth deficits compared to constitutive JA-overproducing mutants.
Perspectives
This project was exciting as it connected several very different experimental approaches and, with this, fostered many fruitful collaborations. For instance, for the first time, we were able to link electrophysiology directly with genetics by employing chloroplasts isolated from Arabidopsis mutants. In addition, we performed detailed transcriptomics, quantified hormone levels, and ultimately tested and verified our hypothesis by infecting plants with pathogens and monitoring their resistance. Taken together, all this data allowed us to tie a simple channel mediating cation flux across the chloroplast envelope to a physiological defense outcome affecting the entire plant. Our work was driven by one key ambition: can we learn to decode plastid calcium signals to ultimately make use of them? With PECs, we now have a first handle to understanding that the plastid calcium code can be shaped to adjust plant stress signaling. This opens up future strategies that aim to precisely tune plant stress signaling and boost plant defense when they need it the most.
Hans-Henning Kunz
Ludwig-Maximilians-Universitat Munchen
Read the Original
This page is a summary of: PLASTID ENVELOPE ION CHANNELS (PEC1/2) link Ca
2+
and jasmonic acid signaling in plant cells, Proceedings of the National Academy of Sciences, August 2026, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2525536123.
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