Opposite Roles of Salicylic Acid Receptors NPR1 and NPR3/NPR4 in Transcriptional Regulation of Plant Immunity
Salicylic acid (SA) is a plant defense hormone required for immunity. Arabidopsis NPR1 and NPR3/NPR4 were previously shown to bind SA and all three proteins were proposed as SA receptors. NPR1 functions as a transcriptional co-activator, whereas NPR3/NPR4 were suggested to function as E3 ligases tha...
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Veröffentlicht in: | Cell 2018-05, Vol.173 (6), p.1454-1467.e15 |
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Sprache: | eng |
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Zusammenfassung: | Salicylic acid (SA) is a plant defense hormone required for immunity. Arabidopsis NPR1 and NPR3/NPR4 were previously shown to bind SA and all three proteins were proposed as SA receptors. NPR1 functions as a transcriptional co-activator, whereas NPR3/NPR4 were suggested to function as E3 ligases that promote NPR1 degradation. Here we report that NPR3/NPR4 function as transcriptional co-repressors and SA inhibits their activities to promote the expression of downstream immune regulators. npr4-4D, a gain-of-function npr4 allele that renders NPR4 unable to bind SA, constitutively represses SA-induced immune responses. In contrast, the equivalent mutation in NPR1 abolishes its ability to bind SA and promote SA-induced defense gene expression. Further analysis revealed that NPR3/NPR4 and NPR1 function independently to regulate SA-induced immune responses. Our study indicates that both NPR1 and NPR3/NPR4 are bona fide SA receptors, but play opposite roles in transcriptional regulation of SA-induced defense gene expression.
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•SA receptors NPR3 and NPR4 function redundantly as transcriptional co-repressors•SA inhibits the transcriptional repression activities of SA receptors NPR3/NPR4•NPR1 and NPR4 have opposite roles in early defense gene expression in response to SA•NPR4 and NPR1 function in parallel to regulate SA-induced defense gene expression
Salicylic acid receptors NPR1 and NPR3/NPR4 play opposite roles in the transcriptional regulation of plant defense against pathogens. |
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ISSN: | 0092-8674 1097-4172 |
DOI: | 10.1016/j.cell.2018.03.044 |