Two studies conducted in the laboratory of Alexander von Humboldt Professor
Jijie Chai at the Max Planck Institute for Plant Breeding Research provide
unprecedented structural insight into how plant immune receptors are primed
and activated to provide plants with resistance against microbial pathogens.


An important plant mechanism is defined by cytoplasmic receptors called NLRs
that recognize effectors, the molecules that invading microorganisms secrete
into the plant's cells. These recognition events can either involve direct
recognition of effectors by NLRs or indirect recognition, in which the NLRs
act as 'guards' that monitor additional host proteins or 'guardees' that are
modified by effectors.

The studies by Jijie Chai together with research teams from Tsinghua
University and the Chinese Academy of Sciences have now pieced together the
sequence of molecular events that convert inactive NLR molecules into active
complexes that provide disease resistance.

The researchers looked at the protein called ZAR1, an ancient plant molecule
capable of indirectly sensing several unrelated bacterial effectors. They
observed that in the absence of bacterial effectors, ZAR1, together with
RKS1, stays in a latent state through interactions involving multiple
domains of the ZAR1 protein. Upon infection, a bacterial effector modifies
the plant 'guardee' PBL2, which then activates RKS1 resulting in huge
conformational changes that first allow plants to swap ADP for ATP and then
result in the assembly of a pentameric, wheel-like structure that the
authors term the 'ZAR1 resistosome'.

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