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MoErv29 promotes apoplastic effector secretion contributing to virulence of the rice blast fungus Magnaporthe oryzae

During plant-pathogenic fungi and host plants interactions, numerous pathogen-derived proteins are secreted resulting in the activation of the unfolded protein response (UPR) pathway. For efficient trafficking of secretory proteins, including those important in disease progression, the cytoplasmic coat protein complex II (COPII) exhibits a multifunctional role whose elucidation remains limited.

Bin QianXiaotong SuZiyuan YeXinyu LiuMuxing LiuDanyu ShenHan ChenHaifeng ZhangPing WangZhengguang Zhang

New Phytol.; 2022 Feb; 233(3):1289-1302.  doi: 10.1111/nph.17851. Epub 2021 Nov 26.

Abstract

During plant-pathogenic fungi and host plants interactions, numerous pathogen-derived proteins are secreted resulting in the activation of the unfolded protein response (UPR) pathway. For efficient trafficking of secretory proteins, including those important in disease progression, the cytoplasmic coat protein complex II (COPII) exhibits a multifunctional role whose elucidation remains limited. Here, we discovered that the COPII cargo receptor MoErv29 functions as a target of MoHac1, a previously identified transcription factor of the UPR pathway. In Magnaporthe oryzae, deletion of MoERV29 severely affected the vegetative growth, conidiation and biotrophic invasion of the fungus in susceptible rice hosts. We demonstrated that MoErv29 is required for the delivery of secreted proteins through recognition and binding of the amino-terminal tripeptide motifs following the signal peptide. By using bioinformatics analysis, we predicted a cargo spectrum of MoErv29 and found that MoErv29 is required for the secretion of many proteins, including extracellular laccases and apoplastic effectors. This secretion is mediated through the conventional endoplasmic reticulum-Golgi secretion pathway and is important for conferring host recognition and disease resistance. Taken together, our results revealed how MoErv29 operates on effector secretion, and our findings provided a critical link between COPII vesicle trafficking and the UPR pathway.

 

See https://pubmed.ncbi.nlm.nih.gov/34761375/

 

Figure 4: MoErv29 is important for suppressing the production of host reactive oxygen species (ROS). (a) 3,3′‐Diaminobenzidine (DAB) staining on infected barley cells of CO39 with Guy11, ∆Moerv29 mutants, and the complement strains at 24 h post‐inoculation (hpi). Bar, 10 μm. (b) Graphics represents the percentage of the invaded barley cells (n = 100) stained by DAB. Error bars represent ± SD; *, P < 0.01. (c, d) Diphenyleneiodonium (DPI) treatment was used to inhibit the activity of nicotinamide adenine dinucleotide phosphate oxidases, which are necessary generators of plant ROS. Dimethyl sulphoxide treatment was a control that is used to dissolve DPI. Bar, 10 μm. (e, f) Expression analysis of defence‐related genes by quantitative real‐time PCR at 24 and 48 hpi. The average threshold cycle of triplicate reactions was normalised to elongation factor 1a (EF1a, Os03g08020) in O. sativa. Three independent biological experiments were performed and yielded similar results. Error bars represent ± SD; asterisks represent significant differences (*, P < 0.01).

 

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