Magnaporthe oryzae causes blast disease, which is one of the most devastating infections in rice and several important cereal crops.

Magnaporthe oryzae needs to coordinate gene regulation, morphological changes, nutrient acquisition and host evasion in order to invade and proliferate within the plant tissues. Thus far, the molecular mechanisms underlying the regulation of invasive growth in planta have remained largely unknown. We identified a precise filamentous-punctate-filamentous cycle in mitochondrial morphology during Magnaporthe-rice interaction. Interestingly, disruption of such mitochondrial dynamics by deletion of genes regulating either the mitochondrial fusion (MoFzo1) or fission (MoDnm1) machinery, or inhibition of mitochondrial fission using Mdivi-1 caused significant reduction in M. oryzae pathogenicity. Furthermore, exogenous carbon source(s) but not antioxidant treatment delayed such mitochondrial dynamics/transition during invasive growth. In contrast, carbon starvation induced the breakdown of the mitochondrial network and led to more punctate mitochondria in vitro. Such nutrient-based regulation of organellar dynamics preceded MoAtg24-mediated mitophagy, which was found to be essential for proper biotrophic development and invasive growth in planta. We propose that precise mitochondrial dynamics and mitophagy occur during the transition from biotrophy to necrotrophy and are required for proper induction and establishment of the blast disease in rice.





Figure 1: Specific changes in mitochondrial morphology during in planta growth of Magnaporthe oryzae. (a) Mitochondrial morphology in M. oryzae during infection. The conidial suspension of the MitoGFP strain was inoculated on rice sheath (Oryza sativa cultivar CO39). Confocal microscopy was carried at 30, 48 and 72 h post‐inoculation (hpi). The 3D reconstruction of the mitochondrial morphology was performed in Bitplan Imaris. Red spots and green filaments represent punctate and filamentous mitochondria, respectively. Scale bar: 8 μm. (b) Quantification of the different morphologies of mitochondria in the wild‐type MitoGFP strain during infection. Error bars represent mean ± SD from three independent replicates. Sample size is more than 200 appressoria penetration sites/host tissue per analysis.