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. 2017 May 4;12(5):e1313378.
doi: 10.1080/15592324.2017.1313378. Epub 2017 Apr 7.

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

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

Bianca Genenncher et al. Plant Signal Behav. .

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.

Keywords: Arabidopsis immunity; LysM-RLK; NUP88/MOS7; PRR; cell death; cerk1–4; nucleocytoplasmic transport; nucleoporin.

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Figures

Figure 1.
Figure 1.
The mos7–1 mutation suppresses the stunted growth morphology and deregulated cell death response of the CHITIN ELICITOR RECEPTOR KINASE1 mutant cerk1–4. (A) Morphology of 8-week-old unchallenged plants of the indicated genotypes grown on soil under an 8 h photoperiod. Scale bar: 1 cm. (B) Cell death response of leaves inoculated with the non-host fungal pathogen Blumeria graminis f.sp hordei (Bgh). 5-week-old leaves were stained with lactophenol trypan blue 9 d post inoculation (dpi) to visualize plant cell death. Scale bar: 500 µm. Backgrounds are Col-3 gl1 for cerk1–4 and Col-0 for mos7–1 and the T-DNA knockout mutant cerk1–2. Experiments were performed twice with similar results.

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