Conserved Opposite Functions in Plant Resistance to Biotrophic and Necrotrophic Pathogens of the Immune Regulator SRFR1.

Jae-Yean Kim,Uyen Thi Vuong,Jiyun Moon,Walter Gassmann,Rahul Mahadev Shelake,Sang Hee Kim,Geon Hui Son,Robert A. Ingle

doi:10.3390/ijms22126427

Abstract

Plant immunity is mediated in large part by specific interactions between a host resistance protein and a pathogen effector protein, named effector-triggered immunity (ETI). ETI needs to be tightly controlled both positively and negatively to enable normal plant growth because constitutively activated defense responses are detrimental to the host. In previous work, we reported that mutations in SUPPRESSOR OF rps4-RLD1 (SRFR1), identified in a suppressor screen, reactivated EDS1-dependent ETI to Pseudomonas syringae pv. tomato (Pto) DC3000. Besides, mutations in SRFR1 boosted defense responses to the generalist chewing insect Spodoptera exigua and the sugar beet cyst nematode Heterodera schachtii. Here, we show that mutations in SRFR1 enhance susceptibility to the fungal necrotrophs Fusarium oxysporum f. sp. lycopersici (FOL) and Botrytis cinerea in Arabidopsis. To translate knowledge obtained in AtSRFR1 research to crops, we generated SlSRFR1 alleles in tomato using a CRISPR/Cas9 system. Interestingly, slsrfr1 mutants increased expression of SA-pathway defense genes and enhanced resistance to Pto DC3000. In contrast, slsrfr1 mutants elevated susceptibility to FOL. Together, these data suggest that SRFR1 is functionally conserved in both Arabidopsis and tomato and functions antagonistically as a negative regulator to (hemi-) biotrophic pathogens and a positive regulator to necrotrophic pathogens.

Highlights

Plants are exposed to a wide variety of potential pathogens and developed a plethora of strategies aimed at protection
Arabidopsis srfr1 mutants were mainly involved in ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1)-dependent effector-triggered immunity (ETI) responses against pv. tomato (Pto) DC3000 [4,6,13] and in the resistance to chewing insect S. exigua and the sugar beet cyst nematode H. schachtii, which is an obligate biotrophic pathogen [10]
The srfr1-1 and the srfr1-2 mutants displayed enhanced susceptibility to FOL compared to RLD, as reflected by more severe symptoms, such as increased chlorosis (Figure 1a), increased lesion size (Figure 1b), and intense hyphal development (Figure 1c)

Summary

Introduction

Plants are exposed to a wide variety of potential pathogens and developed a plethora of strategies aimed at protection. The plant immune response consists of two layers. The first layer is pattern-triggered immunity (PTI), which is induced by microbe- or pathogenassociated molecular patterns (MAMPs or PAMPs), the conserved structural molecules associated with microbial organisms, such as chitin, flagellin, and EF-Tu [1]. Recognition of MAMPs/PAMPs by pattern recognition receptors (PRRs) transduces signals to trigger downstream immune responses, such as activation of MAPK cascades, regulation of transcription factors, and expression of defense-related genes, leading to the limitation of pathogen spread and colonization [1,2]. In turn, evolved a second layer of defense using resistance proteins (R) to monitor pathogen effectors, called effector-triggered immunity (ETI). Many plant R proteins contain nucleotide-binding (NB) and leucine-rich repeat (LRR) domains, called

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