Selective Degradation of Mitochondria by Mitophagy in Pathogenic Fungi

Selective mitochondrial autophagy or mitophagy is an evolutionarily conserved cellular process that selectively degrades superfluous, damaged, and dysfunctional mitochondria. This process is believed to be a mitochondrial quality control system crucial for intracellular homeostasis. Recently, researchers developed a range of methods to induce mitophagy and a variety of assays to monitor this process. With these new methods, the research on mitophagy has been developed rapidly. In particular, some key receptors and regulatory factors in fungi have been identified, which provides a basis for further understanding of the mechanism of this process. Although it has been studied extensively in the model yeast Saccharomyces cerevisiae, mitophagy in pathogenic fungi remains poorly understood. However recent studies have shown that mitophagy is involved in the regulation of pathogenicity of pathogenic fungi, which greatly increases the importance of mitophagy. Therefore, it is necessary to review the current research on mitophagy in order to provide an accurate understanding of mitophagy and promote mitophagy research in the pathogenic fungi.

Two H3K36 methyltransferases differentially associate with transcriptional activity and enrichment of facultative heterochromatin in rice blast fungus

Di-and tri-methylation of lysine 36 on histone H3(H3K36me2/3)is catalysed by histone methyltransferase Set2,which plays an essential role in transcriptional regulation.Although there is a single H3K36 methyltransferase in yeast and higher eukaryotes,two H3K36 methyltransferases,Ash1 and Set2,were present in many filamentous fungi.However,their roles in H3K36 methylation and transcriptional regulation remained unclear.Combined with methods of RNA-seq and ChIP-seq,we revealed that both Ash1 and Set2 are redundantly required for the full H3K36me2/3 activity in Magnaporthe oryzae,which causes the devastating worldwide rice blast disease.Ash1 and Set2 distinguish genomic H3K36me2/3-marked regions and are differentially associated with repressed and activated transcription,respectively.Furthermore,Ash1-catalysed H3K36me2 was co-localized with H3K27me3 at the chromatin,and Ash1 was required for the enrichment and transcriptional silencing of H3K27me3-occupied genes.With the different roles of Ash1 and Set2,in H3K36me2/3 enrichment and transcriptional regulation on the stress-responsive genes,they differentially respond to various stresses in M.oryzae.Overall,we reveal a novel mechanism by which two H3K36 methyltransferases catalyze H3K36me2/3 that differentially associate with transcriptional activities and contribute to enrichment of facultative heterochromatin in eukaryotes.

The E3 ubiquitin ligase OsRGLG5 targeted by the Magnaporthe oryzae effector AvrPi9 confers basal resistance against rice blast

Rice blast,caused by Magnaporthe oryzae,is one of the most devastating diseases of rice.During infection,M.oryzae secretes effectors to facilitate blast development.Among these effectors,the avirulence factor AvrPi9 is recognized by Pi9,a broad-spectrum blast resistance protein that triggers Pi9-mediated resistance in rice.However,little is known about the interaction between AvrPi9 and Pi9 and how AvrPi9 exerts virulence to promote infection.In this study,we found that ectopic expression of AvrPi9 in the Pi9-lacking cultivar TP309 suppressed basal resistance against M.oryzae.Furthermore,we identified an AvrPi9-interacting protein in rice,which we named OsRGLG5,encoding a functional RING-type E3 ubiquitin ligase.During infection,AvrPi9 was ubiquitinated and degraded by OsRGLG5.Meanwhile,AvrPi9 affected the stability of OsRGLG5.Infection assays revealed that OsRGLG5 is a positive regulator of basal resistance against M.oryzae,but it is not essential for Pi9-mediated blast resistance in rice.In conclusion,our results revealed that OsRGLG5 is targeted by the M.oryzae effector AvrPi9 and positively regulates basal resistance against rice blast.

Warm temperature compromises JA-regulated basal resistance to enhance Magnaporthe oryzae infection in rice

Changes in global temperatures profoundly affect the occurrence of plant diseases.It is well known that rice blast can easily become epidemic in relatively warm weather.However,the molecular mechanism remains unclear.In this study,we show that enhanced blast development at a warm temperature(22C)compared with the normal growth temperature(28C)is rice plant-determined.Comparative transcriptome analysis revealed that jasmonic acid(JA)biosynthesis and signaling genes in rice could be effectively induced by Magnaporthe oryzae at 28C but not at 22C.Phenotypic analyses of the osaoc1 and osmyc2 mutants,OsCOI1 RNAi lines,and OsMYC2-OE plants further demonstrated that compromised M.oryzaeinduced JA biosynthesis and signaling lead to enhanced blast susceptibility at the warm temperature.Consistent with these results,we found that exogenous application of methyl jasmonate served as an effective strategy for improving blast resistance under the warm environmental conditions.Furthermore,decreased activation of JA signaling resulted in the downregulated expression of some key basal resistance genes at 22C when compared with 28C.Among these affected genes,OsCEBiP(chitin elicitorbinding protein precursor)was found to be directly regulated by OsMYB22 and its interacting protein OsMYC2,a key component of JA signaling,and this contributed to temperature-modulated blast resistance.Taken together,these results suggest that warm temperature compromises basal resistance in rice and enhances M.oryzae infection by reducing JA biosynthesis and signaling,providing potential new strategies for managing rice blast disease under warm climate conditions.