The Arabidopsis-turnip crinkle virus (TCV) system is one of the few tractable plant-virus systems that allow simultaneous characterization of host components required for basal- and/or resistance (R) protein-mediated defenses. Another unique feature is that hypersensitive response (HR) and resistance can be studied as two distinct phenotypes in this pathosytem. The R protein HRT confers HR to TCV but requires a recessive locus rrt to confer resistance. The pathways leading to HR and resistance are mutually exclusive. HRT interacts with EDS1, which potentiates HR to TCV and is also required for resistance signaling. HRT-mediated signaling is also dependent on the EDS1-interacting proteins PAD4 and SAG101, which form binary and ternary complexes with EDS1. HRT-mediated resistance is also dependent on light and more specifically on the blue-light photoreceptors, cryptochromes (CRY) and phototropins (PHOT). Of these, CRY2 and PHOT2 are required for the stability of HRT. HRT is degraded in a proteasome-dependent manner, which correlates with its interaction with the E3 ubiquitin ligase, COP1. Together, these results suggest that components of light signaling modulate plant defense against TCV by regulating the stability of, and signaling mediated by, the R protein HRT.