Atypical E2F Transcriptional Repressor DEL1 Acts at the Intersection of Plant Growth and Immunity by Controlling the Hormone Salicylic Acid

In plants, the activation of immunity is often inversely correlated with growth. Mechanisms that control plant growth in the context of pathogen challenge and immunity are unclear. Investigating Arabidopsis infection with the powdery mildew fungus, we find that the Arabidopsis atypical E2F DEL1, a transcriptional repressor known to promote cell proliferation, represses accumulation of the hormone salicylic acid (SA), an established regulator of plant immunity. DEL1-deficient plants are more resistant to pathogens and slightly smaller than wild-type. The resistance and size phenotypes of DEL1-deficient plants are due to the induction of SA and activation of immunity in the absence of pathogen challenge. Moreover, Enhanced Disease Susceptibility 5 (EDS5), a SA transporter required for elevated SA and immunity, is a direct repressed target of DEL1. Together, these findings indicate that DEL1 control of SA levels contributes to regulating the balance between growth and immunity in developing leaves. [Display omitted] •Atypical E2F DEL1 misexpression alters G. orontii growth and pathogenesis in Arabidopsis•DEL1-deficient plants (del1-1) are smaller and more resistant to G. orontii•Altered size and resistance of del1-1 is due to elevated basal salicylic acid (SA)•DEL1 directly targets EDS5, a SA transporter required for elevated SA and immunity Investigating powdery mildew infection in Arabidopsis, Chandran et al. uncover a function for a conserved eukaryotic atypical E2F transcription repressor, DEL1, in restraining immunity. During leaf development, DEL1, a known promoter of cell proliferation, acts directly to repress defense hormone salicylic acid accumulation, thereby suppressing plant immunity and maximizing growth.