The molecular mechanism of SUMO modification inhibiting the continuous immune response of plants.

In order to successfully infect plants, pathogens often inhibit the host's immune response by injecting effect proteins into plant cells.
plant's NOD-type receptor (NLRs) specifically identifies the effect protein and stimulates the immune response (ETI) triggered by the effects.
but the continuous activation of immune response when no pathogen strain is detrimental to the normal growth and development of plants.
SUMO modification is a protein translation modification, which affects protein activity, stability, interaction, intracellular positioning, etc.
studies have shown that SUMO-mediated SUMO modification mediated by SUMO E3 connective sIZ1 may inhibit the ongoing immune response, but its molecular regulatory mechanism is not clear.
Jin Jingbo research group of the Institute of Botany of the Chinese Academy of Sciences, with amoeba as the research object, revealed the mechanism of SIZ1 regulating plant immune response by SUMO modified transcription inhibitor TPR1.
TPR1 and NLR protein SNC1 and histone deacetylase (HDA19) form a complex that regulates the immune response mediated by SNC1.
researchers found that SUMO E3 connectivee SIZ1 interacted with TPR1 and mediated its SUMO modification, and sIZ1-mediated SUMO modification inhibited the transcription altrusion of TPR1 and TPR1-HDA19, and maintained the SNC1/TPR1 complex in an inactive state.
in SIZ1 mutants, THE SUMO modification of TPR1 was inhibited, resulting in transcription inhibition of TPR1 and the enhancement of TPR1-HDA19, thus activating the sNC1/TPR1-mediated immune response.
this study reveals the molecular mechanism of SUMO modification inhibiting the continuous immune response of plants, which is of great significance for the normal growth and development of plants under normal conditions.
the study was published online December 11 in the international academic journal Molecular Plant.
Jin Jingbo Research Group, Ph.D. Niu De is the first author of the thesis, Jin Jingbo is the communication author of this paper.
the research was supported by the National Natural Science Foundation of China and the Chinese Academy of Sciences.
Source: Plant Research Institute.