ER retention receptor, MoERR1 is required for fungal development and pathogenicity in the rice blast fungus, Magnaporthe oryzae

Abstract

ER retention receptor is a seven trans-membrane protein that plays pivotal roles in function and integrity of endoplasmic reticulum (ER). Insertional mutagenesis of Magnaporthe oryzae identified MoERR1 as a pathogenicity gene encoding putative ER retention receptor orthologous to ERD2 in Saccharomyces cerevisiae. Search through the genome identified that M. oryzae possesses another ortholog of ERD2, which is designated as MoERR2. When MoERR1 and MoERR2 were tagged with GFP, both were localized to ER. Targeted disruption of MoERR1 showed pleiotropic effects on phenotypes, while deletion of MoERR2 had no effect on phenotypes we examined. The disruption mutant of MoERR1 showed growth retardation and produced significantly reduced number of conidia with aberrant morphology. Appressoria from the mutant were unable to penetrate into plant tissues presumably due to defect in cell wall integrity, thereby rendering the mutant non-pathogenic. The MoERR1 mutant also appeared to display abnormal ER structure and mis-regulation of genes involved in chaperone function and unfolded protein response under ER stress condition. Taken together, these results suggest that MoERR1 is a ER retention receptor required for function and integrity of ER, and that MoERR1-mediated ER functionalities are essential for fungal development and pathogenesis.

MoMCP1, a Cytochrome P450 Gene, Is Required for Alleviating Manganese Toxin Revealed by Transcriptomics Analysis in Magnaporthe oryzae

“…The Gene ontology (GO) enrichment and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis were used for further analysis (Figures S3 and S4). To explore the compromised pathogenicity in the ∆ Momcp1 mutant, we determined many pathogenicity related genes in our RNA-seq results, and there are many genes regulated in the ∆ Momcp1 mutant (Figure 6, Table 1) [23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46]. Interestingly, several surface and signal recognition genes showed much higher or lower expression levels than the other pathogenicity related genes, indicating that the expressions of these genes were regulated in the ∆ Momcp1 mutant.…”

Multi-omics analysis revealed that the protein kinase MoKin1 affected the cellular response to endoplasmic reticulum stress in the rice blast fungus, Magnaporthe oryzae

“…Some mutants of proteins localizing in the ER, such as MoSCS2, MoSpf1, MoERR1 and MoLHS1, could also cause ER stress and reduced the pathogenicity. ER stress was also involved in the regulation of signal transduction [25,[34][35][36]. For example, in S. cerevisiae, the ER and cell wall were coordinated by UPR and CWI signaling pathways to protect cells from the effects of some stressors [37].…”

The SNARE Protein CfVam7 Is Required for Growth, Endoplasmic Reticulum Stress Response, and Pathogenicity of Colletotrichum fructicola

“…Overaccumulation of misfolded or unfolded proteins, or dysregulation of sterols or lipids, could trigger the ER stress and influence the expression of specific genes. Such responses are known as unfolded protein responses (UPRs) ( Tang et al, 2015 ; Goh et al, 2017 ). UPR is essential for the pathogenesis of pathogens, and bZIP transcription factor Hac1 participates in the processes of UPR ( Tang et al, 2015 ).…”