Divergent pathogen effectors promote virulence by manipulating a transcriptional node of growth-defense crosstalk
L. YANG (1), P. José Pereira Lima Teixeira (1), S. Biswas (2), Y. He (3), O. Finkel (4), M. English (5), P. Epple (6), P. Mieczkowski (4), J. Dangl (7) (1) University of North Carolina Chapel Hill, U.S.A.; (2) Harvard Medical School, U.S.A.; (3) NC State University, U.S.A.; (4) University of North Carolina Chapel Hill, U.S.A.; (5) University of Tennessee, U.S.A.; (6) BASF Plant Science LP, U.S.A.; (7) University of North Carolina Chapel Hill; HHMI, U.S.A.

Active defense response is usually associated with an expense of fast growth, which is known as the ‘growth-defense tradeoff’ phenomenon. Plants strategically regulate the output of phytohormone signaling network to balance these two vital processes. Effector proteins derived from pathogens can physically interact with host cellular components to attenuate defense response or redirect resource allocation. We identified TCP14, a known transcriptional regulator of plant growth, as a convergent target of effectors from three different pathogens, Golovinomyces orontii, Pseudomonas syringae (Psy), Hyaloperonospora arabidopsidis (Hpa), and showed that it is required for intact immunity. Here, we demonstrate that TCP14 contributes to full immunity as a repressor of a subset of Jasmonic acid (JA) response. tcp14 mutations enhance the susceptibility to Hpa, and rescue the growth defects of Pto DC3000 cor-. We provide mechanistic examples showing that bacterial and oomycete effectors promote virulence by differentially manipulating TCP14. A Psy type III effector, HopBB1 promotes TCP14 degradation via the SCFCOI1-complex by connecting it to JAZ3, a repressor of the JA pathway. Transcriptome and physiology data indicate that HopBB1 fine tunes host phytohormone crosstalk by precisely manipulating subsets of both the TCP14 and MYC regulons to avoid pleiotropic host responses, while still promoting pathogen proliferation. Interestingly, a TCP14-interacting Hpa effector (HaRxL45) alters its function through a different mechanism, resulting in dwarfism.

Abstract Number: P16-481
Session Type: Poster