Abstract
Activation of systemic acquired resistance in plants is associated with transcriptome reprogramming induced by the unstable coactivator NPR1. Immune-induced ubiquitination and proteasomal degradation of NPR1 are thought to facilitate continuous delivery of active NPR1 to target promoters, thereby maximising gene expression. Because of this potentially costly sacrificial process, we investigated if ubiquitination of NPR1 plays transcriptional roles prior to its proteasomal turnover. Here we show ubiquitination of NPR1 is a progressive event in which initial modification by a Cullin-RING E3 ligase promotes its chromatin association and expression of target genes. Only when polyubiquitination of NPR1 is enhanced by the E4 ligase, UBE4, it is targeted for proteasomal degradation. Conversely, ubiquitin ligase activities are opposed by UBP6/7, two proteasome-associated deubiquitinases that enhance NPR1 longevity. Thus, immune-induced transcriptome reprogramming requires sequential actions of E3 and E4 ligases balanced by opposing deubiquitinases that fine-tune activity of NPR1 without strict requirement for its sacrificial turnover.
Highlights
Immune responses must be tightly controlled to provide appropriate, efficient and timely resistance to pathogenic threats
To examine if stepwise ubiquitination of NPR1 plays a role in plant immune responses we examined a potential role for E4 ligases
In agreement with the gene expression data, enhanced susceptibility was maintained in ube4 ics1 double mutants (Figure 1D), indicating the autoimmune phenotype of adult ube4 plants is completely dependent on salicylic acid (SA)
Summary
Immune responses must be tightly controlled to provide appropriate, efficient and timely resistance to pathogenic threats. A major hallmark of eukaryotic immune responses is dramatic reprogramming of the transcriptome to prioritise defences over other cellular functions. In plants transcriptional reprogramming is largely orchestrated by the immune hormone salicylic acid (SA) that accumulates upon recognition of biotrophic pathogens. Establishment of SAR and associated transcriptome reprogramming are mediated by the transcriptional coactivator NPR1 (nonexpressor of pathogenesisrelated (PR) genes 1). The majority of SA-induced genes are NPR1 dependent, indicating NPR1 is a master regulator of plant immunity (Wang et al, 2006). Loss of NPR1 function results in severely immune-compromised plants unable to activate SAR
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