Salicylic acid (SA)-mediated plant immunity against biotic stresses: An insight on molecular components and signaling mechanism

植物免疫 水杨酸 机制(生物学) 生物逆境 免疫 化学 生物 计算生物学 细胞生物学 免疫系统 生物化学 免疫学 非生物胁迫 物理 突变体 基因 拟南芥 量子力学
作者
Sapna Mishra,Rajib Roychowdhury,Shatrupa Ray,Alkesh Hada,Ajay Kumar,Umakanta Sarker,Tariq Aftab,Ranjan Das
出处
期刊:Plant Stress [Elsevier BV]
卷期号:11: 100427-100427 被引量:85
标识
DOI:10.1016/j.stress.2024.100427
摘要

Since the beginning of the 21st century, climate change has been pervasive. Such climatic instabilities not only trigger plants' adaptability and survivability in harsh environments, but also sustain the spread of a broad spectrum of pathogens including bacteria, fungi, and viruses, that create disease pressure by affecting plant health and the immune barrier. Salicylic acid (SA) is a potent phytohormone and signaling molecule that plays pivotal roles in physio-biochemical processes during plant development. In addition to its widely known role in abiotic stress response, SA also plays a vital role in plants' immune response to biotic stresses through their signaling pathways, molecular interactions, and corresponding interactions with other phytohormones like jasmonic acid, ethylene, abscisic acid, etc. In this perspective, signaling response is dictated by a plethora of SA interacting genes, proteins, and transcription factors (TFs). The genes and genetic regulators (TFs and regulatory proteins) are associated with SA signaling to fine-tune plants' immune response through activating systemic and localized signaling cascade, triggering genes for pathogenesis-related (PR) proteins, phytoalexins, etc., to modulate pathogen effectors. In this way, SA boosts the plant's immune system through systemic acquired resistance (SAR) and induced systemic resistance (ISR). In addition, gene editing and epigenetic regulation of SA-responsive genes are valuable innovative tools to understand and decipher the complex molecular SA-involved mechanism and its future utilities to make climate-adaptive plants with broad spectrum resistance.
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