Salicylic acid inhibits V-ATPase activity and restricts cell elongation

  • While the role of salicylic acid (SA) in plant defence has been investigated for decades, its role in regulating plant growth and development has only come into focus recently. SA application inhibits growth independently of the established “Nonexpressor of Pathogenesis Related” (NPR) receptors. However, the underlying mechanism at the cellular level remains largely elusive. Here, we show that SA induces changes in vacuolar morphology and a significant increase in vacuolar pH in Arabidopsis (Arabidopsis thaliana). We demonstrate SA-mediated inhibition of V-ATPase activity, which is confirmed by experiments using the V-ATPase mutant vha-a2 vha-a3. The observed effects seem to be independent of the phytohormone auxin, which has been reported to crosstalk with SA. By inhibiting V-ATPase activity, SA impacts basic cellular functions such as vesicle trafficking and/or nutrient storage, affecting cell size and growth. Our results reveal a NPR-independent mechanism that attenuates growth, potentially reallocating resources to enhance plant robustness and promote endurance during environmental stresses.

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Author:Jonas Müller, Yvonne König, Kaltra Xhelilaj, Sabrina Kaiser, Tobias Müller, Alejandra Vielba-Fernández, Julien Gronnier, Christian Löfke, Melanie Krebs, David ScheuringORCiD
URN:urn:nbn:de:hbz:386-kluedo-96538
ISSN:1532-2548
Parent Title (English):Plant Physiology
Publisher:Oxford University Press
Document Type:Article
Language of publication:English
Date of Publication (online):2025/09/26
Year of first Publication:2025
Publishing Institution:Rheinland-Pfälzische Technische Universität Kaiserslautern-Landau
Date of the Publication (Server):2026/02/26
Issue:199 / 2
Article Number:kiaf439
Page Number:14
Source:10.1093/plphys/kiaf439
Faculties / Organisational entities:Kaiserslautern - Fachbereich Biologie
DDC-Cassification:5 Naturwissenschaften und Mathematik / 570 Biowissenschaften, Biologie
Collections:Open-Access-Publikationsfonds
Licence (German):Lizenz nach Originalpublikation