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Pathogen perception

One of the things I found most fascinating when I studied biology as an undergradraduate student was our immune system. More precisely the process by which we make specific antibodies that can recognize a seemingly endless number of epitopes. This system seemed so perfect that I did not imagine how an organism could survive without it. It turns out that plants do not have antibodies to defend themselves. This is most remarkable since plants are sessile organisms and therefore cannot escape from pathogens or adverse conditions and yet, many plants can outlive humans, and must therefore fight pathogens as we do.

To most people plants may seem less complex than human but they have developed a very powerful, efficient and complex immune system that we are just starting to understand. In addition to physical barriers plants possess two lines of defense. The first is mediated by pathogen recognition receptors (PRR), which are cell surface receptor that recognize pathogen-associated molecular pattern (PAMP) which are common between several pathogens. Once activated, the receptor triggers a low intensity defense response, named PAMP-triggered immunity (PTI). In most case this is sufficient to thwart the pathogen attack.

However, pathogen possess an array of virulence factors that specifically target the PRR or downstream components of the PTI and try to suppress it. If the pathogen  successfully suppress PTI then it may win the fight and colonize the plant. But the plant still has a last weapon: Resistance protein (R). These plant proteins can recognize virulence factors (or their effect) and trigger a very powerful response that includes the activation of MAP kinases, the discharge of reactive oxygen species, an elevated salicylic acid level and generally culminates in the hypersensitive response, a type of cell death aimed at preventing the growth of the pathogen. Since R proteins activation can mean death for the cell, their expression and activation must be tightly regulated.

I am mostly interested by PAMP perception by PRR, the suppression of the PRR by virulence genes, the recognition of virulence factors by R proteins and the cellular localization and activation of R proteins.