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Review summarizes salicylic acid's role in regulating cell survival during senescence and pathogen responses, suggesting implications for plant immunity.
Salicylic acid (SA) is a crucial plant hormone synthesized via two primary pathways: the ISOCHORISMATE SYNTHASE (ICS) pathway and the PHENYLALANINE AMMONIA-LYASE (PAL) pathway. SA biosynthesis and homeostasis are precisely regulated in plants. Furthermore, SA functions in a concentration-dependent manner to enhance resistance to both abiotic stresses and pathogens, as well as to regulate plant senescence. However, the underlying mechanisms of SA action remain to be elucidated. Recent studies have demonstrated that in juvenile plants, age-related cues, autoimmunity, and autophagy contribute to maintaining SA at the basal level. In adult plants, moderate concentrations of SA enhance resistance by activating autophagy and the antioxidant system in response to abiotic stresses and pathogen infections. Elevated levels of SA initiate positive feedback loop involving reactive oxygen species (ROS) and the transcriptional regulator WRKY75, which serves as a core regulatory hub during natural senescence, abiotic stress-induced premature senescence, and pathogen infection-triggered hypersensitive response (HR). In the late stages of these processes, autophagy acts synergistically with high levels of SA to accelerate programmed cell death (PCD). This review summarizes recent advancements in SA biosynthesis and compares the associated signaling pathways during plant senescence and pathogen infection, providing theoretical insights into SA-regulated plant senescence and immunity.
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Luo et al. (2026) studied this question.
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