Date of this Version
Virology. 2014 January 20; 449: 207–214
Turnip crinkle virus (TCV) has been shown to interact with a NAC transcription factor, TIP, of Arabidopsis thaliana, via its coat protein (CP). This interaction correlates with the resistance response manifested in TCV-resistant Arabidopsis ecotype Di-17. We report that failure of a mutated CP to interact with TIP triggered the corresponding TCV mutant (R6A) to cause more severe symptoms in the TCV-susceptible ecotype Col-0. We hypothesized that TCV regulates antiviral basal immunity through TIP-CP interaction. Consistent with this hypothesis, we found that the rate of accumulation of R6A was measurably slower than wild-type TCV over the course of an infection. Notably, R6A was able to accumulate at similar rates as wild-type TCV in mutant plants with defects in salicylic acid (SA) signaling. Finally, plants with altered TIP expression provided evidence R6A's inability to evade the basal resistance response was likely associated with loss of ability for CP to bind TIP.
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