Effector-dependent rewiring of tomato bHLH transcription circuits alters plant growth and immunity during Xanthomonas infection.
Y. SUN (1), J. Kim (2), M. Mudgett (2) (1) Stanford Biology, U.S.A.; (2) Stanford, U.S.A.

XopD is a non-TAL type III secretion effector that directly represses host transcription during Xanthomonas euvesicatoria (Xcv) infection. XopD encodes a small ubiquitin-like modifier (SUMO) protease that suppresses ethylene (ET) and salicylic acid (SA) production to interfere with host immune signaling. Nothing is known about how plants recognize XopD and activate defense. Given that XopD manipulates transcription, we hypothesized that host transcription triggered but not repressed by XopD may define defense pathways effective for anti-Xcv immunity. Using this rationale, we identified a tomato basic helix-loop-helix (bHLH) transcription factor (TF) that is differentially expressed by XopD in a SUMO-protease-dependent manner. Most notably, qRT-PCR shows that basal mRNA levels of the tomato bHLH TF (DH1) are very low in leaves, high in roots, but becomes highly increased in leaves in a XopD-dependent manner during Xcv infection. DH1 transcripts increase in leaves in response to PAMPs, stress hormones, and gene-for-gene interactions suggesting a role during PTI and ETI. Genetic and biochemical studies revealed that DH1 is a DNA-binding protein that is required for immunity in leaves, as well as normal vegetative growth. Interestingly, stable DH1-silencing resulted in stunted growth, shorter internodes, reduced leaf expansion, smaller leaves, and reduced root density. To gain insight to how DH1 transcription is regulated in response to growth and defense signals, we generated transgenic, tomato GUS reporter lines expressing different regions of the DH1 promoter. We identified a 500bp region in the DH1 promoter that is responsive to PAMP, hormone treatment, and XopD perturbation. Taken together, our work suggests that tomato DH1 plays an important role in tomato growth and defense. We will report progress in characterizing the DH1-dependent transcription network and the mechanism(s) by which TF-modules regulate DH1 transcription during normal growth and Xcv infection.

Abstract Number: P9-309
Session Type: Poster