ArticlePlant physiology2026
JrCDPK13L-mediated phosphorylation of JrERF113L promotes walnut resistance to Colletotrichum gloeosporioides.
Article in Plant physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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