Nucleoporin NUP88/MOS7 is required for manifestation of phenotypes associated with the Arabidopsis CHITIN ELICITOR RECEPTOR KINASE1 mutant cerk1–4

Abstract

Arabidopsis nucleoporin MOS7/NUP88 was identified in a forward-genetic screen for components that contribute to auto-immunity of the deregulated Resistance (R) gene mutant snc1, and is required for immunity to biotrophic and hemi-biotrophic pathogens. In a recent study, we showed that MOS7 is also essential to mount a full defense response against the necrotrophic fungal pathogen Botrytis cinerea, suggesting that MOS7 modulates plant defense responses to different types of pathogenic microbes. Here, we extend our analyses of MOS7-dependent plant immune responses and report the genetic requirement of MOS7 for manifestation of phenotypes associated with the CHITIN ELICITOR RECEPTOR KINASE1 (CERK1) mutant cerk1-4. KEYWORDSArabidopsis immunity; cell death; cerk1-4; LysM-RLK; NUP88/MOS7; nucleoporin; nucleocytoplasmic transport; PRRThe plant innate immune system relies on 2 major classes of immune receptors to detect pathogens and activate downstream defense responses. At the plasma membrane, pattern recognition receptors (PRRs) recognize conserved pathogen-or microbe-associated molecular patterns (PAMPs/MAMPs) such as fungal chitin via extracellular ligand binding domains, whereas intracellular nucleotide-binding site leucine-rich repeat receptors (NLRs) perceive the action of specific pathogen effector molecules. 1 Cellular defense signaling upon activation of both immune receptor classes involves the relay of stress stimuli into the nucleus to alter the expression of immune response genes. [2][3][4] The macromolecular exchange across the nuclear envelope (NE) is regulated by nuclear transport receptors (NTRs) and nuclear pore complexes (NPCs) composed of nucleoporins (Nups). 5,6 In Arabidopsis, the NUP88 homolog MOS7 (MODIFIER OF SNC1, 7) was first identified in a forward-genetic screen for positive regulators of auto-immunity activated in the deregulated Toll-Interleukin Receptor (TIR)-type NLR mutant suppressor of npr1-1, constitutive1 (snc1). 7 Whereas snc1 plants are dwarf, accumulate high levels of the defense hormone salicylic acid (SA), constitutively express PATHOGENESIS RELATED (PR) genes and show enhanced resistance to virulent biotrophic and hemi-biotrophic pathogens, 8,9 these phenotypes are abolished in snc1 mos7-1 double mutant plants. 7 Subsequent analyses showed that mos7-1 single mutants are impaired in nuclear retention of auto-active SNC1 as well as the SA response regulators ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) and NONEXPRESSOR OF PATH-OGENESIS-RELATED GENES1 (NPR1). Accordingly, mos7-1 shows defects in SA-, EDS1-and NPR1-dependent immunity to virulent and avirulent isolates of the biotrophic oomycete Hyaloperonospora arabidopsidis and the hemi-biotrophic bacterium Pseudomonas syringae. 7,10 More recently, we uncovered that MOS7 is also essential for establishing a full defense response against the gray mold fungus Botrytis cinerea, a necrotrophic pathogen that kills its host plants. 11 When co-expressed transiently in leaves of Nicotiana benthamiana, MOS7 interacts with NUP98a and N...

Identification of Arabidopsis genes involved in differential interaction phenotype establishment by distinct Verticillium spp. and isolates

“…MPK3 is a component of a MAP kinase cascade which leads to induction of pathogenesis related genes, whereas MOS7 represents a nucleoporin protein which is required for selective nuclear retention of immune regulatory proteins (Cheng et al, 2009; al., 2010; Mao et al, 2011). Both proteins were shown to be required for defence responses to B. cinerea (Ren et al, 2008;Genenncher et al, 2017). The mean diameter of necrotic lesions on at5g24080-1 leaves was not significantly altered as compared to Col-0 wild-type (Fig.…”

Two cysteine-rich receptor-like protein kinases, CRK7 and CRK43, are required for CERK1-4 dependent cell death responses in Arabidopsis thaliana

“…Moreover it was shown that the nucleoporin NUP88, also known as MODIFIER OF SNC1 7 (MOS7) is necessary for cerk1-4 cell death since cerk1-4 mos7-1 double mutants are lacking the exaggerated cell death response. This indicates that formation of the cerk1-4 cell death requires downstream signal transduction into the nucleus and MOS7-dependent nuclear accumulation of regulatory proteins (Genenncher et al, 2017).…”

“…A potential candidate for nuclear import of CRK43 is MOS7, a nucleoporin that was shown to be necessary for cerk1-4 cell death induction (Genenncher et al, 2017).…”