Cell Host Microbe 19, 204–215 (2016)

The immune response in plants is costly because every cell defends itself, so it is only induced when pathogen presence is sensed through membrane or cytosolic receptors. NLRs are cellular sensors that perceive the presence or activity of pathogen effectors being delivered into the plant cell, initiating a strong immune response. If this control is lost, defence can be constitutively switched on and plants then suffer from autoimmunity, leading to dwarfed growth.

To find new immune regulators that may be difficult to discover in a wild-type background, Shuai Huang, Xin Li and colleagues from the University of British Columbia, Canada, searched for mutations that enhanced the autoimmune phenotype of the mutant snc1, in which the NLR protein SNC1 is stabilized. They identified two redundant TRAF-like proteins named MUSE. TRAFs are major players in animal immunity, and despite the large family in Arabidopsis, these proteins have been seldom studied in plants. A double muse mutant shows very severe autoimmune symptoms, confirming the role of MUSE proteins as negative regulators of immunity.

After an elegant series of genetic and molecular experiments, the authors concluded that, just like in animals, the two MUSE proteins mediate the formation of signalling complexes called TRAFasomes, which bring together NLRs and proteasome components. These complexes control NLR homeostasis, so that plants can choose between growth and defence.