Unveiling exogenous potential of phytohormones as sustainable arsenals against plant pathogens: molecular signaling and crosstalk insights

Abstract

Plants frequently confront pathogens that disrupt physiological and molecular functions, ultimately reducing agricultural yields. To counter these challenges, plants activate sophisticated defense mechanisms to recognize stress signals while optimizing growth. Phytohormones signaling pathways and their crosstalk are central to regulating plant growth, development and defense. Numerous proteins associated with phytohormone signaling pathways have been identified, including receptors for several vital hormones. Previous studies indicate that defense phytohormones, like salicylic acid (SA), jasmonic acid (JA) and ethylene (ET), are crucial to pathogen defense. SA specifically mediates systemic acquired resistance against biotrophic pathogens, while induced systemic resistance relies on JA and ET signaling in response to necrotrophic pathogens. Other hormones, typically associated with growth and development, such as ethylene, abscisic acid, brassinosteroids, melatonin, gibberellins, auxin, and cytokinin, also interact in a complex network of synergistic and antagonistic relationships with defense phytohormones. Moreover, they can achieve effects that surpass conventional pathogen control methods, suggesting their potential as exogenous biocontrol agents. During the past decade, our knowledge of hormone signaling and stress response has become immense. Thus, this review is an attempt to summarize some of the advances in plant signaling and crosstalk mechanisms as well as their potential to be a future arsenal in biotic stress mitigation strategies. Ultimately, this work emphasizes using exogenous phytohormones as a viable alternative for controlling pathogens to enhance crop productivity in pathogen-affected regions.

Keywords: Biotic stress; Exogenous biofertilizers; Metabolic regulation; Molecular mechanisms; Phytohormones; Plant defense systems; Plant physiology; Transcription inducers.