CPL1/FRY2 Regulates ABA Biosynthesis and Modulates SA/JA-Mediated Defence in Arabidopsis.
TL;DR
It is demonstrated that CPL1 regulates ABA biosynthesis and modulates SA/JA-associated defence responses in Arabidopsis thaliana, positioning CPL1 as a key integrator of epigenetic regulation, hormone crosstalk, and pathogen-specific immune tuning.
Abstract
The RNA polymerase II C-terminal domain (CTD) phosphatase CPL1/FRY2 is a multifunctional regulator involved in diverse stress responses, yet its role in orchestrating hormone-mediated immunity remains poorly understood. Here, we demonstrate that CPL1 regulates ABA biosynthesis and modulates SA/JA-associated defence responses in Arabidopsis thaliana. Loss of CPL1 function compromises resistance to the hemibiotrophic bacterial pathogen Pseudomonas syringae pv. tomato DC3000 (Pst DC3000), coinciding with suppressed SA signalling and ectopic activation of JA-, ethylene-, and abscisic acid (ABA)-responsive genes. Hormone profiling revealed that upon Pst DC3000 infection, cpl1 mutants specifically accumulated ABA, but not SA, JA, or ethylene. Epistasis analyses showed that this ABA accumulation stems from the derepression of the seed-specific transcription factor FUSCA3 (FUS3) in vegetative tissues, which in turn drives expression of the ABA biosynthetic gene NCED3. Chromatin immunoprecipitation analyses further revealed that FUS3 silencing in wild-type plants is maintained by repressive epigenetic marks, including low histone acetylation and high H3K9me2/3 levels, modifications that are disrupted in cpl1 mutants. Consequently, CPL1 promotes resistance to biotrophic/hemibiotrophic pathogens by epigenetically silencing FUS3 to prevent pathogen-induced ABA biosynthesis, thereby modulating SA/JA-associated defence responses. Our findings position CPL1 as a key integrator of epigenetic regulation, hormone crosstalk, and pathogen-specific immune tuning.