JrCDPK13L-mediated phosphorylation of JrERF113L promotes walnut resistance to Colletotrichum gloeosporioides
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Published on: May 21, 2019
Haiyi Yu1, Yuhui Dong1, Kun Zhang1
1College of Forestry, Shandong Agricultural University, Tai'an, Shandong 271000, China.
Abstract:
Walnut anthracnose caused by Colletotrichum gloeosporioides poses a serious threat to the walnut industry. Calcium-dependent protein kinases (CDPKs) are critical regulators that transmit calcium (Ca2+) signals into cellular immune responses. However, the specific functional mechanisms of CDPKs in walnut resistance to anthracnose infection remain unclear. In this study, we identified and characterized JrCDPK13L as a positive regulator of anthracnose resistance in walnut, acting in a Ca2+-dependent manner through transcriptomic, genetic, and molecular biology assays. Mechanistically, JrCDPK13L interacts with the ethylene-responsive factor JrERF113L, which was shown to promote walnut resistance to anthracnose based on disease resistance evaluation in transgenic strains. Furthermore, JrCDPK13L phosphorylates JrERF113L at Ser271/280 residues, which enhances both the protein stability and disease resistance of JrERF113L. In addition, JrERF113L directly binds to the promoter regions and activates the transcription of pathogenesis-related gene JrPR5L, and this activation is further strengthened by the JrCDPK13L-mediated phosphorylation of JrERF113L at Ser271/280. Collectively, our findings reveal a novel signaling module, JrCDPK13L-JrERF113L-JrPR5L, that enhances walnut resistance to anthracnose, providing significant insights into the role of Ca2+ signaling pathways in woody plant immunity.
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