Linker histone variant HIS1-3 and WRKY1 oppositely regulate salt stress tolerance in Arabidopsis.

The salt overly sensitive (SOS) pathway plays an important role in plant salt stress; however, the transcriptional regulation of the genes in this pathway is unclear. In this study, we found that Linker histone variant HIS1-3 and WRKY1 oppositely regulate the salt stress response in Arabidopsis (Arabidopsis thaliana) through the transcriptional regulation of SOS genes. The expression of HIS1-3 was inhibited by salt stress, and the disruption of HIS1-3 resulted in enhanced salt tolerance. Conversely, the expression of WRKY1 was induced by salt stress, and the loss of WRKY1 function led to increased salt sensitivity. The expression of SOS1, SOS2, and SOS3 was repressed and induced by HIS1-3 and WRKY1, respectively, and HIS1-3 regulated the expression of SOS1 and SOS3 by occupying the WRKY1 binding sites on their promoters. Moreover, WRKY1 and HIS1-3 acted upstream of the SOS pathway. Together, our results indicate that HIS1-3 and WRKY1 oppositely modulate salt tolerance in Arabidopsis through transcriptional regulation of SOS genes.

AtWRKY1 negatively regulates the response of Arabidopsis thaliana to Pst. DC3000.

WRKY transcription factors (TFs) play a major role in resistance to plant diseases, but the role of AtWRKY1 in response to Pst. DC3000 is not clear. In this study, we found that AtWRKY1 negatively affected the response of Arabidopsis to Pst. DC3000. During Pst. DC3000 infection, the transcription of AtWRKY1 was suppressed. The wrky1 mutants displayed enhanced resistance to Pst. DC3000. In contrast, the overexpression of AtWRKY1 reduced the resistance. The relative RNA levels of defense related PR genes were increased in the loss-of-function mutants, whereas their expressions were decreased in the AtWRKY1-overexpressing plants. Further research revealed that salicylic acid (SA) can repress the expression of AtWRKY1, and overexpression of AtWRKY1 weakened the SA-mediated defense response. In addition, the AtWRKY1 protein can bind to the PR1 promoter in vivo and in yeast cells directly, thereby inhibiting the transcription of PR1. AtWRKY1 indirectly represses the expression of PR2 and PR5. Our results indicated that the AtWRKY1 gene negatively regulates the plant defense responses to Pst. DC3000 through SA signaling pathways.