Pathogen effector disarms circadian-immune crosstalk by targeting TCP14, a dual regulator of clock and defense

Pathogens across kingdoms converge on hijacking plant immune hubs, but why certain host proteins emerge as evolutionary "hotspots" remains elusive. Here, we reveal that the transcription factor TCP14, a prime effector target, serves as a circadian-immune integrator. The clock components CCA1 and ZTL orchestrate TCP14 levels through transcriptional activation and proteasomal degradation, respectively, generating diurnal oscillations in TCP14 activity. Reciprocally, TCP14 promotes the transcription of several clock genes by directly binding to their promoters. Time-course RNA-seq and genetic analyses demonstrated that TCP14 plays a broad role in regulating rhythmic gene expression, hypocotyl growth, and time-of-day-specific defense responses. Moreover, a pathogen effector, HaRxL21, directly interacts with TCP14 and transcriptional repressors TPL/TPR1 to suppress defense genes, perturbing time-gated defense. Our work establishes TCP14 as a chrono-immune nexus whose vulnerability arises from its role in coupling circadian timing to defense prioritization, offering a paradigm for how pathogens disrupt host rhythms through hub sabotage.