As staple food crops, cereals are essential to feed the world’s growing population. Keeping pace with demography and global change requires increasing cereal yields in a sustainable manner. Destructive fungal pathogens such as Magnaporthe oryzae, the causal agent of the blast disease, represent major threats to cereal production. In this context, the ii-MAX project will produce ground-breaking knowledge of fungal virulence and plant immunity that will be valuable to engineer durable resistance to blast in cereals.
During plant infection, pathogens deploy molecular weapons known as effectors that target cellular processes of the host to promote infection. In M. oryzae, a particularly large and diverse family of effectors has recently been discovered: the MAX (Magnaporthe AVRs and ToxB-like) effector family. Remarkably, these effectors possess various protein sequences but exhibit a conserved structure. The MAX effector family is specific to ascomycete fungi but has undergone massive expansion in M. oryzae suggesting a primary role for these effectors in the infectious process. Nonetheless, the cellular mechanisms they target in cereals are largely unknown. The aim of my project is to identify the host proteins targeted by M. oryzae MAX effectors and conduct a comprehensive study of the biophysical and functional interactions between MAX effectors and their target proteins in rice. This will enable new sources of resistance to be developed by modifying host susceptibility proteins targeted by MAX effectors.
To achieve this goal, I defined four objectives:
1-Identify the host proteins targeted by MAX effectors.
2-Define the structural and biophysical properties governing the interaction of MAX effectors with their virulence targets in cereals.
3-Improve resistance to blast in rice by mutating virulence targets of MAX effectors required for susceptibility to M. oryzae.
4-Elucidate the virulence function of MAX effectors through functional investigation of their targets.
Fields of science
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