Transcriptional responses of wild-type and zin1 mutant Arabidopsis plants to infection with Pseudomonas syringae

Phytopathogens use secreted effector proteins to suppress host immunity and promote pathogen virulence, and there is increasing evidence that the host-pathogen interactome comprises a complex network. In an effort to identify novel interactors of the Pseudomonas syringae effector HopZ1a, we performed a yeast two-hybrid screen that identified a previously uncharacterized Arabidopsis protein that we designate HopZ1a Interactor 1 (ZIN1). Additional analyses in yeast and in planta revealed that ZIN1 also interacts with several other P. syringae effectors. We show that an Arabidopsis loss-of-function zin1 mutant is less susceptible to infection by certain strains of P. syringae, while overexpression of ZIN1 results in enhanced susceptibility. Functionally, ZIN1 exhibits topoisomerase-like activity in vitro. Transcriptional profiling of wild-type and zin1 Arabidopsis plants inoculated with P. syringae indicated that ZIN1 regulates a wide range of pathogen-responsive biological processes, although the list of genes more highly expressed in zin1 versus wild-type plants was particularly enriched for ribosomal protein genes. Altogether, these data illuminate ZIN1 as a potential susceptibility hub that interacts with multiple effectors to influence the outcome of plant-microbe interactions. Wild-type and zin1 mutants infiltrated with either 10 mM MgCl2 (Control), 1 x 10^8 cfu/mL Pseudmonas syringae pv. tomato DC3000, or 1 x 10^8 cfu/mL P. syringae pv. tomato DC3000 ΔhrcC (three biological replicates each for a total of 18 samples)