Molecular regulation of the salicylic acid hormone pathway in plants under changing environmental conditions

• Published in: Trends in biochemical sciences (Amsterdam. Regular ed.) Vol. 48; no. 8; pp. 699 - 712
• Main Authors: Rossi, Christina A.M., Marchetta, Eric J.R., Kim, Jong Hum, Castroverde, Christian Danve M.
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.08.2023
• Subjects: Arabidopsis - metabolism; Arabidopsis Proteins - metabolism; cell signaling; climate change; gene regulation; Hormones - metabolism; plant hormone; plant immunity; salicylic acid; Salicylic Acid - metabolism; Transcription Factors - metabolism; plant hormone; salicylic acid; gene regulation; plant immunity; cell signaling; climate change
• ISSN: 0968-0004; 1362-4326
• DOI: 10.1016/j.tibs.2023.05.004

Salicylic acid (SA) is an aromatic plant hormone mediating plant growth, development, and immunity, including local and systemic defenses against pathogens and pests.Research for the past three decades has advanced our understanding of the SA pathway, from metabolic enzymes and receptors to signaling components and gene regulation.Key components of SA biosynthesis, signaling, metabolism, and transport are impacted by changing abiotic (e.g., temperature, water availability) and biotic factors (e.g., commensal and beneficial microbes).Temperature regulation of the SA pathway has led to the discovery of major thermosensitive nodes at various levels of gene/protein regulation.Microbiome modulation of the SA pathway at the single species and community levels are being disentangled, revealing mechanisms that rely on canonical plant hormone crosstalk. Salicylic acid (SA) is a central plant hormone mediating immunity, growth, and development. Recently, studies have highlighted the sensitivity of the SA pathway to changing climatic factors and the plant microbiome. Here we summarize organizing principles and themes in the regulation of SA biosynthesis, signaling, and metabolism by changing abiotic/biotic environments, focusing on molecular nodes governing SA pathway vulnerability or resilience. We especially highlight advances in the thermosensitive mechanisms underpinning SA-mediated immunity, including differential regulation of key transcription factors (e.g., CAMTAs, CBP60g, SARD1, bHLH059), selective protein–protein interactions of the SA receptor NPR1, and dynamic phase separation of the recently identified GBPL3 biomolecular condensates. Together, these nodes form a biochemical paradigm for how the external environment impinges on the SA pathway.