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An endolysosomal pathway controls cytoplasmic accumulation of helper immune receptors in an NLR network

Cian Duggan: Imperial College London

<div>In asterids, a complex signalling network of nucleotide-binding leucine-rich repeat (NLR) proteins mediates resistance to viruses, nematodes, bacteria and oomycetes. In this network, the helper NLR NRC4 pairs with sensor NLRs, such as Rpi-blb2, Mi-1.2 and Rx, to mediate hypersensitive response (HR) and immunity. The molecular mechanisms that regulate NRC4 protein turnover are uncharacterized. We hypothesized that NRC4 protein levels must be tightly regulated to ensure an appropriate level of immunity. To investigate this, we identified NRC4 interactors by mass spectrometry. We found that NRC4 associates with components of vesicle transport regulators and vacuolar sorting adaptors implicated in lysosomal degradation. Knocking-down some of these interactors altered NRC4 protein stability and the HR triggered by an autoactive NRC4 mutant. Overexpression of some of these proteins suppressed NRC4 triggered HR, consistent with their putative roles in promoting NRC4 degradation. Notably, this pathway controlled protein accumulation of other NRC helpers but not NLRs outside the NRC clade. Our results implicate a vacuolar degradation pathway in regulating helper NLR protein accumulation and immunity. This could enable plants to avoid unwarranted immune activation under normal conditions and maintain optimal levels of helper-sensor NLRs in a complex network. Strategic fine-tuning of this pathway could improve broad-spectrum disease resistance to diverse plant pathogens.</div>

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