NPR1 Promotes Its Own and Target Gene Expression in Plant Defense by Recruiting CDK8
NPR1 (NONEXPRESSER OF PR GENES1) functions as a master regulator of the plant hormone salicylic acid (SA) signaling and plays an essential role in plant immunity. In the nucleus, NPR1 interacts with transcription factors to induce the expression of ( - ) genes and thereby promote defense responses....
Gespeichert in:
Veröffentlicht in: | Plant physiology (Bethesda) 2019-09, Vol.181 (1), p.289-304 |
---|---|
Hauptverfasser: | , , , , , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | NPR1 (NONEXPRESSER OF PR GENES1) functions as a master regulator of the plant hormone salicylic acid (SA) signaling and plays an essential role in plant immunity. In the nucleus, NPR1 interacts with transcription factors to induce the expression of
(
-
) genes and thereby promote defense responses. However, the underlying molecular mechanism of
gene activation is poorly understood. Furthermore, despite the importance of NPR1 in plant immunity, the regulation of
expression has not been extensively studied. Here, we show that SA promotes the interaction of NPR1 with both CDK8 (CYCLIN-DEPENDENT KINASE8) and WRKY18 (WRKY DNA-BINDING PROTEIN18) in Arabidopsis (
). NPR1 recruits CDK8 and WRKY18 to the
promoter, facilitating its own expression. Intriguingly, CDK8 and its associated Mediator subunits positively regulate
and
expression and play a pivotal role in local and systemic immunity. Moreover, CDK8 interacts with WRKY6, WRKY18, and TGA transcription factors and brings RNA polymerase II to
and
promoters and coding regions to facilitate their expression. Our studies reveal a mechanism in which NPR1 recruits CDK8, WRKY18, and TGA transcription factors along with RNA polymerase II in the presence of SA and thereby facilitates its own and target gene expression for the establishment of plant immunity. |
---|---|
ISSN: | 0032-0889 1532-2548 |
DOI: | 10.1104/pp.19.00124 |