Nuclear Pore Complex Component MOS7/Nup88 Is Required for Innate Immunity and Nuclear Accumulation of Defense Regulators inArabidopsis   

Abstract

Plant immune responses depend on dynamic signaling events across the nuclear envelope through nuclear pores. Nuclear accumulation of certain resistance (R) proteins and downstream signal transducers are critical for their functions, but it is not understood how these processes are controlled. Here, we report the identification, cloning, and analysis of Arabidopsis thaliana modifier of snc1,7 (mos7-1), a partial loss-of-function mutation that suppresses immune responses conditioned by the autoactivated R protein snc1 (for suppressor of npr1-1, constitutive 1). mos7-1 single mutant plants exhibit defects in basal and R protein-mediated immunity and in systemic acquired resistance but do not display obvious pleiotropic defects in development, salt tolerance, or plant hormone responses. MOS7 is homologous to human and Drosophila melanogaster nucleoporin Nup88 and resides at the nuclear envelope. In animals, Nup88 attenuates nuclear export of activated NF-kB transcription factors, resulting in nuclear accumulation of NF-kB. Our analysis shows that nuclear accumulation of snc1 and the defense signaling components Enhanced Disease Susceptibility 1 and Nonexpresser of PR genes 1 is significantly reduced in mos7-1 plants, while nuclear retention of other tested proteins is unaffected. The data suggest that specifically modulating the nuclear concentrations of certain defense proteins regulates defense outputs.

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

“…11 Together, these data show that MOS7/NUP88 is an important regulator of multiple immune response pathways against (hemi-)biotrophic and necrotrophic pathogens and suggest that MOS7 modulates plant immune responses at the level of the NPC according to the particular type of pathogen attacking. 7,11 In Arabidopsis, perception of the fungal cell wall polysaccharide MAMP chitin is mediated by the lysin motif receptor-like kinase (LysM-RLK), CHITIN ELICITOR RECEP-TOR KINASE1 (CERK1). 12,13 A mutated version of this PRR, PLANT SIGNALING & BEHAVIOR 2017, VOL.…”

“…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 NUP98b, 2 phenylalanine-glycine (FG)-repeat nucleoporins implicated in maintaining the selective permeability barrier of the NPC.…”

“…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).…”

“…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.…”

“…11 Together, these data show that MOS7/NUP88 is an important regulator of multiple immune response pathways against (hemi-)biotrophic and necrotrophic pathogens and suggest that MOS7 modulates plant immune responses at the level of the NPC according to the particular type of pathogen attacking. 7,11 In Arabidopsis, perception of the fungal cell wall polysaccharide MAMP chitin is mediated by the lysin motif receptor-like kinase (LysM-RLK), CHITIN ELICITOR RECEP-TOR KINASE1 (CERK1). 12,13 A mutated version of this PRR, harboring a L 124 F amino acid exchange in its second LysM domain, was isolated from a forward-genetic screen for components that contribute to non-host resistance of Arabidopsis ecotype Col-3 gl1 against the non-adapted barley powdery mildew fungus Blumeria graminis f.sp.…”