TaWRKY50-TaSARK7 module-mediated cysteine-rich protein phosphorylation suppresses the programmed cell death response to Chinese wheat mosaic virus infection
WRKY transcription factors are widely involved in plant responses to biotic and abiotic stresses. However, there is currently a limited understanding of the regulation of viral infection by WRKY transcription factors in wheat (Triticum aestivum). The WRKY transcription factor TaWRKY50 in group IIb w...
Gespeichert in:
Veröffentlicht in: | Virology (New York, N.Y.) N.Y.), 2024-07, Vol.595, p.110071, Article 110071 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
Zusammenfassung: | WRKY transcription factors are widely involved in plant responses to biotic and abiotic stresses. However, there is currently a limited understanding of the regulation of viral infection by WRKY transcription factors in wheat (Triticum aestivum). The WRKY transcription factor TaWRKY50 in group IIb wheat exhibited a significant response to Chinese wheat mosaic virus infection. TaWRKY50 is localized in the nucleus and is an activating transcription factor. Interestingly, we found that silencing TaWRKY50 induces cell death following inoculation with CWMV. The protein kinase TaSAPK7 is specific to plants, whereas NbSRK is a closely related kinase with high homology to TaSAPK7. The transcriptional activities of both TaSAPK7 and NbSRK can be enhanced by TaWRKY50 binding to their promoters. CRP is an RNA silencing suppressor. Furthermore, TaWRKY50 may regulate CWMV infection by regulating the expression of TaSAPK7 and NbSRK to increase CRP phosphorylation and reduce the amount of programmed cell death (PCD).
•TaWRKY50 play a negative role in the regulation of CWMV resistance in wheat.•The transcription level of both TaSAPK7 and NbSRK can be enhanced by binding TaWRKY50 to their promoters.•TaWRKY50 promote CWMV infection by enhancing CRP phosphorylation to reduce programmed cell death (PCD). |
---|---|
ISSN: | 0042-6822 1096-0341 1096-0341 |
DOI: | 10.1016/j.virol.2024.110071 |