WRKY transcription factors (TFs) play crucial roles in plant resistance responses to pathogens. Wheat stripe rust, caused by the fungal pathogen Puccinia striiformis f. sp. tritici (Pst), is a destructive disease of wheat (Triticum aestivum) worldwide. In this study, the two WRKY genes TaWRKY49 and TaWRKY62 were originally identified in association with high-temperature seedling-plant resistance to Pst (HTSP) resistance in wheat cultivar Xiaoyan 6 by RNA-seq. Interestingly, the expression levels of TaWRKY49 and TaWRKY62 were down- and up-regulated, respectively, during HTSP resistance in response to Pst. Silencing of TaWRKY49 enhanced whereas silencing TaWRKY62 reduced HTSP resistance. The enhanced resistance observed on leaves following the silencing of TaWRKY49 was coupled with increased expression of salicylic acid (SA)- and jasmonic acid (JA)-responsive genes TaPR1.1 and TaAOS, as well as reactive oxygen species (ROS)-associated genes TaCAT and TaPOD; whereas the ethylene (ET)-responsive gene TaPIE1 was suppressed. The decreased resistance observed on leaves following TaWRKY62 silencing was associated with increased expression of TaPR1.1 and TaPOD, and suppression of TaAOS and TaPIE1. Furthermore, SA, ET, MeJA (methyl jasmonate), hydrogen peroxide (H2O2) and abscisic acid (ABA) treatments increased TaWRKY62 expression. On the other hand, MeJA did not affect the expression of TaWRKY49, and H2O2 reduced TaWRKY49 expression. In conclusion, TaWRKY49 negatively regulates while TaWRKY62 positively regulates wheat HTSP resistance to Pst by differential regulation of SA-, JA-, ET and ROS-mediated signaling.
Stripe rust, caused by Puccinia striiformis f. sp. tritici (Pst), is a destructive disease of wheat worldwide. The disease is preferably controlled by growing resistant cultivars. Wheat cultivar Xiaoyan 6 (XY 6) has been resistant to stripe rust since its release. In the previous studies, XY 6 was found to have higher-temperature seedling-plant (HTSP) resistance. However, the molecular mechanisms of HTSP resistance were not clear. To identify differentially expressed genes (DEGs) involved in HTSP resistance, we sequenced 30 cDNA libraries constructed from XY 6 seedlings exposed to several temperature treatments. Compared to the constant normal (15°C) and higher (20°C) temperature treatments, 1395 DEGs were identified in seedlings exposed to 20°C for 24 h (to activate HTSP resistance) and then kept at 15°C. These DEGs were located on all 21 chromosomes, with 29.2% on A, 41.1% on B and 29.7% on D genomes, by mapping to the Chinese Spring wheat genome. The 1395 DEGs were enriched in ribosome, plant-pathogen interaction and glycerolipid metabolism pathways, and some of them were identified as hub proteins (phosphatase 2C10), resistance protein homologs, WRKY transcription factors and protein kinases. The majority of these genes were up-regulated in HTSP resistance. Based on the differential expression, we found that phosphatase 2C10 and LRR receptor-like serine/threonine protein kinases are particularly interesting as they may be important for HTSP resistance through interacting with different resistance proteins, leading to a hypersensitive response.
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