Résumé
The interaction between rice and the blast fungus
Magnaporthe grisea is the focus of extensive studies on rice disease resistance and fungal infection mechanisms. Here, we review the characteristics of susceptible rice blast infections in terms of physiology, cytology and both host and pathogen transcriptional responses. The success of the infection and the type of disease symptoms strongly depend on environmental and developmental cues. After its penetration into a host cell, the fungus differentiates invasive hyphae that fill up the plant cell lumen and are in direct contact with the membrane of the infected cell. The infected plant cell is alive, displaying considerable vesicle accumulation near the fungus, which is consistent with the establishment of a biotrophic phase at this stage of the infection. Colonization of host tissues by the fungus occurs through the perforation of cell walls from adjacent cells, likely using plasmodesmata as breaking points, or through hyphal growth in the apoplasm. After a few days of biotrophic growth within rice tissues, the fungus switches to a necrotrophic-like phase associated with the onset of sporulation, leading to visible lesions. Genome-wide transcriptomic studies have shown that classical plant defence responses are triggered during a susceptible infection, although the kinetics and amplitude of these responses are slower and lower than in resistant interactions. Infected rice cells are submitted to an intense transcriptional reprogramming, where responses to hormones such as auxins, abscissic acid and jasmonates are likely involved. Consistent with the extensive plant–fungal exchanges during the biotrophic phase, many rice genes expressed during infection encode plasma membrane proteins. At the onset of lesion formation (5 days after the start of infection),
M. grisea is actively reprogramming its transcription towards active DNA, RNA and protein syntheses to sustain its rapid growth in infected tissues. A striking characteristic of
M. grisea genes expressed at this stage of the infection is the over-representation of genes encoding secreted proteins, mainly of unknown function. However, some of these secreted proteins are enzymes involved in cell wall, protein and lipid degradation, suggesting that the fungus is starting to degrade host polymers and cell walls or is remodelling its own cell wall. The next challenge will be to decipher the role of these induced plant and fungal genes in the susceptible interaction.