Molecules and Cells

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Fig. 2.

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Fig. 2. (A) In rpm1 mutant plants, the type III effectors, AvrRpm1 and AvrB, phosphorylate RIN4 to promote bacterial growth. ROC1 isomerizes RIN4P149 and inhibits RPS2. (B) In resistant plants, ROC1 suppresses RPM1 and RPS2. RIN4 phosphorylation at the T166 residue removes ROC1 suppression and activates RPM1. RPM1 activation initiates a hypersensitive response and decreases bacterial growth. AvrPphB inhibits AvrB-induced RPM1 activation. (C) The type III effector AvrRpt2 cleaves RIN4 upon delivery and processing. In rps2 mutant plants, AvrRpt2 cleaves RIN4 to promote bacterial growth. RIN4 cleavage subsequently decreases the accumulation of RPM1. (D) In resistant plants, RIN4 degradation activates RPS2, which initiates hypersensitive response and decreases bacterial growth. The RIN4–NDR1 association is important for RPS2 activation. RIN4 degradation activates the resistance protein RPS2, and HopF2 inhibits AvrRpt2-mediated RIN4 cleavage. AvrRpt2: , AvrB: , AvrRpm1: , RIPK: , ROC1: , NDR1: .
Mol. Cells 2019;42:503~511 https://doi.org/10.14348/molcells.2019.2433
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