Effector-triggered immunity blocks pathogen degradation of an immunity-associated vesicle traffic regulator in Arabidopsis.

摘要: Innate immunity in plants can be triggered by microbe- and pathogen-associated molecular patterns. The pattern-triggered (PTI) is often suppressed pathogen effectors delivered into the host cell. Plants overcome suppression of PTI reestablish resistance through effector-triggered (ETI). An unanswered question how might pathogen-suppression during ETI. Findings described this paper suggest a possible mechanism. During Pseudomonas syringae pathovar tomato (Pst) DC3000 infection Arabidopsis, ADP ribosylation factor guanine nucleotide exchange factor, AtMIN7, destabilized effector HopM1 26S proteasome. In study, we discovered that AtMIN7 required for not only PTI, consistent with notion Pst degrades to suppress but also level healthy low, increases posttranscriptionally response activation PTI. Whereas led degradation ETI three different effectors, AvrRpt2, AvrPphB, HopA1, Col-0 blocks ability destabilize AtMIN7. Further analyses bacterial translocation stability transgenic show prevents HopM1-mediated inside plant Both are localized trans-Golgi network/early endosome, subcellular compartment previously known associated pathogenesis plants. Thus, blocking endosome-associated critical part mechanism counter