Location: Wheat Health, Genetics, and Quality Research
Title: The leucine-rich repeat receptor-like kinase protein TaSERK1 positively regulates high-temperature seedling plant resistance to Puccinia striiformis f. sp. tritici by interacting with TaDJA7Author
SHI, YIFENG - Northwest A&f University | |
BAO, XIYUE - Northwest A&f University | |
SONG, XIAOPAN - Northwest A&f University | |
LIU, YUYANG - Northwest A&f University | |
LI, YUXIANG - Northwest A&f University | |
Chen, Xianming | |
HU, XIAOPING - Northwest A&f University |
Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal Publication Acceptance Date: 2/7/2023 Publication Date: 2/12/2023 Citation: Shi, Y., Bao, X., Song, X., Liu, Y., Li, Y., Chen, X., Hu, X. 2023. The leucine-rich repeat receptor-like kinase protein TaSERK1 positively regulates high-temperature seedling plant resistance to Puccinia striiformis f. sp. tritici by interacting with TaDJA7. Phytopathology. 113(7):1325-1344. https://doi.org/10.1094/PHYTO-11-22-0429-R. DOI: https://doi.org/10.1094/PHYTO-11-22-0429-R Interpretive Summary: Somatic embryogenesis receptor kinases (SERKs) belongs to the leucine rich repeat – receptor like kinase (LRR-RLK) subfamily, and many LRR-RLKs have been proven to play a key role in plant immune signal transmission. However, the functions of SERKs in resistance to stripe rust remains unknown. Here, we identified a gene, TaSERK1, from Xiaoyan 6 (XY6), a wheat cultivar possessing high-temperature seedling-plant (HTSP) resistance to the fungal pathogen. The expression level of TaSERK1 was up-regulated upon inoculation with the stripe rust pathogen under relatively high temperatures. The transcriptional level of the gene was significantly increased under exogenous salicylic acid and brassinosteroids treatments. Barley stripe mosaic virus - induced gene silencing assay indicated that TaSERK1 positively regulated the HTSP resistance to stripe rust. The transient expression of TaSERK1 in tobacco leaves confirmed its subcellular localization on plasma membrane. Furthermore, TaSERK1 interacted with and phosphorylated the chaperone protein TaDJA7, which belongs to the heat shock protein 40 subfamily. Silencing TaDJA7 compromised the HTSP resistance to stripe rust. The results indicated that when the membrane immune receptor TaSERK1 perceive the dual signal from the rust pathogen infection under relatively high temperatures, it transmitted the signal to TaDJA7 to activate HTSP resistance to the pathogen. The results enhance the understanding of molecular mechanisms of wheat resistance to stripe rust. Technical Abstract: Somatic embryogenesis receptor kinases (SERKs) belongs to the leucine rich repeat – receptor like kinase (LRR-RLK) subfamily, and many LRR-RLKs have been proven to play a key role in plant immune signal transmission. However, the functions of SERKs in resistance to stripe rust caused by Puccinia striiformis f. sp. tritici remains unknown. Here, we identified a gene, TaSERK1, from Xiaoyan 6 (XY6), a wheat cultivar possessing high-temperature seedling-plant (HTSP) resistance to the fungal pathogen. The expression level of TaSERK1 was up-regulated upon P. striiformis f. sp. tritici inoculation under relatively high temperatures. The transcriptional level of TaSERK1 was significantly increased under exogenous salicylic acid (SA) and brassinosteroids (BR) treatments. Barley stripe mosaic virus -induced gene silencing assay indicated that TaSERK1 positively regulated the HTSP resistance to stripe rust. The transient expression of TaSERK1 in tobacco leaves confirmed its subcellular localization on plasma membrane. Furthermore, TaSERK1 interacted with and phosphorylated the chaperone protein TaDJA7, which belongs to the heat shock protein 40 (Hsp40) subfamily. Silencing TaDJA7 compromised the HTSP resistance to stripe rust. The results indicated that when the membrane immune receptor TaSERK1 perceive the dual signal from P. striiformis f. sp. tritici infection under relatively high temperatures, it transmitted the signal to TaDJA7 to activate HTSP resistance to the pathogen. |