Insights into the role of jasmonic acid-mediated defenses against necrotrophic and biotrophic fungal pathogens

doi:10.1007/s11515-011-1171-1

Front Biol

2012, Vol. 7

Issue (1) : 48-56 https://doi.org/10.1007/s11515-011-1171-1

REVIEW

Insights into the role of jasmonic acid-mediated defenses against necrotrophic and biotrophic fungal pathogens

Christopher J. ANTICO, Chad COLON, Taylor BANKS, Katrina M. RAMONELL(

)

Department of Biological Sciences, University of Alabama, Tuscaloosa, AL 35487, USA

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Abstract

Jasmonic acid (JA) is a natural hormone regulator involved in development, responses against wounding and pathogen attack. Upon perception of pathogens, JA is synthesized and mediates a signaling cascade initiating various defense responses. Traditionally, necrotrophic fungi have been shown to be the primary activators of JA-dependent defenses through the JA-receptor, COI1. Conversely, plants infected with biotrophic fungi have classically been associated with suppressing JA-mediated responses. However, recent evidence has shown that certain biotrophic fungal species also trigger activation of JA-mediated responses and mutants deficient in JA signaling show an increase in susceptibility to certain biotrophic fungal pathogens. These findings suggest a new role for JA in defense against fungal biotrophs. This review will focus on recent research advancing our knowledge of JA-dependant responses involved in defense against both biotrophic and necrotrophic fungi.

Keywords jasmonic acid (JA) methyl jasmonate (MeJA) biotrophic fungi necrotrophic fungi COI1

Corresponding Author(s): RAMONELL Katrina M.,Email:kramonel@bama.ua.edu

Issue Date: 01 February 2012

Cite this article:

Christopher J. ANTICO,Chad COLON,Taylor BANKS, et al. Insights into the role of jasmonic acid-mediated defenses against necrotrophic and biotrophic fungal pathogens[J]. Front Biol, 2012, 7(1): 48-56.

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https://academic.hep.com.cn/fib/EN/10.1007/s11515-011-1171-1
https://academic.hep.com.cn/fib/EN/Y2012/V7/I1/48

Fig.1 Schematic Diagram of the JA signaling pathway. JA biosynthesis is initiated by necrotrophic fungal infection, wounding, and herbivory. Once synthesized, derivatives of JA can be modified by JMT making methyl jasmonate and JAR1 with the addition of isoleucine. JA and its derivatives migrate across the nuclear envelope where they are bound by the JA-receptor, COI1. SCF-COI1 complex is activated by JA and specifically targets JAZ proteins (JAZ3 and JAZ1) for protein ubiquitination and subsequent degradation by the proteasome. JAZ proteins are negative regulators of JA-responsive genes. However, once degraded, (also known as ) transcription factor can transcribe JA-responsive genes, which can activate or repress several different functions. The SA-mediated pathway acts antagonistically to repress JA signaling. SA can directly inhibit JA, and activate , which also inhibits JA. Conversely, JA can inhibit SA-mediated responses by suppressing expression through the SCF-COI1 complex. JA signaling can be activated and repressed through other proteins in various pathways. In the MAP kinase cascade, , bound to , can activate JA signaling, but the complex of and can suppress JA-responsive gene, . Red arrows indicate activation. Blue bars indicate suppression. Red dotted arrows indicate binding. Blue dotted arrows indicate degradation. Modified from Kazan and Manners, 2008.

Tab.1 The phenotypes of JA-related mutants when challenged with necrotrophic fungi

Tab.2 The phenotypes of JA-related mutants when challenged with biotrophic fungi

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[1]	Xin YANG, Fengyang DENG, Katrina M. RAMONELL. Receptor-like kinases and receptor-like proteins: keys to pathogen recognition and defense signaling in plant innate immunity[J]. Front Biol, 2012, 7(2): 155-166.

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