Abstract
The Arabidopsis resistance protein HRT recognizes the Turnip crinkle virus (TCV) coat protein (CP) to induce a hypersensitive response (HR) in the resistant ecotype Di-17. The CP also interacts with a nuclear-targeted NAC family of host transcription factors, designated TIP (TCV-interacting protein). Because binding of CP to TIP prevents nuclear localization of TIP, it has been proposed that TIP serves as a guardee for HRT. Here, we have tested the requirement for TIP in HRT-mediated HR and resistance by analyzing plants carrying knockout mutation in the TIP gene. Our results show that loss of TIP does not alter HR or resistance to TCV. Furthermore, the mutation in TIP neither impaired the salicylic acid-mediated induction of HRT expression nor the enhanced resistance conferred by overexpression of HRT. Strikingly, the mutation in TIP resulted in increased replication of TCV and Cucumber mosaic virus, suggesting that TIP may play a role in basal resistance but is not required for HRT-mediated signaling.
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