Progress in Salicylic Acid-Dependent Signaling for Growth-Defense Trade-Off

Abstract

One grand challenge for studying plant biotic and abiotic stress responses is to optimize plant growth and plasticity under variable environmental constraints, which in the long run benefits agricultural production. However, efforts in promoting plant immunity are often accompanied by compromised morphological "syndromes" such as growth retardation, sterility, and reduced yield. Such a trade-off is dictated by complex signaling driven by secondary messengers and phytohormones. Salicylic acid (SA) is a well-known phytohormone essential for basal immunity and systemic acquired resistance. Interestingly, recent updates suggest that external environmental cues, nutrient status, developmental stages, primary metabolism, and breeding strategies attribute an additional layer of control over SA-dependent signaling, and, hence, plant performance against pathogens. In this review, these external and internal factors are summarized, focusing on their specific roles on SA biosynthesis and downstream signaling leading to immunity. A few considerations and future opportunities are highlighted to improve plant fitness with minimal growth compensation.

Keywords: growth–defense trade-off; phytohormones; plant immunity; salicylic acid.

Figure 1

Schematic summary of the connection between different environmental conditions and SA-dependent immunity. Plant growth depends on multiple environmental factors, including temperature, atmospheric CO₂, and soil quality (nutrient status). These factors have also been found to modulate SA level and SA-dependent defense response against various pathogens. Notably, an NPR1-independent pathway exists in external factor-mediated protection, which potentially bypasses SA and the associated negative effect on plant growth. SA, salicylic acid; JA, jasmonic acid; NPR1, nonexpressor of pathoegenesis-related genes 1; PR, pathogenesis-related; Pip, pipecolic acid; NHP, N-hydroxy-pipecolic acid; SAR, systemic acquired resistance; eCO₂, elevated CO₂; P, phosphorus; N, nitrogen; PHR1, phosphate starvation response 1.