Abstract
The potato (Solanum tuberosum) nucleotide binding-leucine-rich repeat immune receptor Rx confers resistance to Potato virus X (PVX) and requires Ran GTPase-activating protein 2 (RanGAP2) for effective immune signaling. Although Rx does not contain a discernible nuclear localization signal, the protein localizes to both the cytoplasm and nucleus in Nicotiana benthamiana. Transient coexpression of Rx and cytoplasmically localized RanGAP2 sequesters Rx in the cytoplasm. This relocation of the immune receptor appeared to be mediated by the physical interaction between Rx and RanGAP2 and was independent of the concomitant increased GAP activity. Coexpression with RanGAP2 also potentiates Rx-mediated immune signaling, leading to a hypersensitive response (HR) and enhanced resistance to PVX. Besides sequestration, RanGAP2 also stabilizes Rx, a process that likely contributes to enhanced defense signaling. Strikingly, coexpression of Rx with the Rx-interacting WPP domain of RanGAP2 fused to a nuclear localization signal leads to hyperaccumulation of both the WPP domain and Rx in the nucleus. As a consequence, both Rx-mediated resistance to PVX and the HR induced by auto-active Rx mutants are significantly suppressed. These data show that a balanced nucleocytoplasmic partitioning of Rx is required for proper regulation of defense signaling. Furthermore, our data indicate that RanGAP2 regulates this partitioning by serving as a cytoplasmic retention factor for Rx.
Highlights
Innate immunity of plants protects them against pathogens and shares several features with animal innate immunity (Ausubel, 2005)
Since the CC domain of GPA2 interacts with Ran GTPase-activating protein 2 (RanGAP2) (Sacco et al, 2007), and because we show that the auto-activity of the G13R45 swap construct, containing the GPA2-CC domain, is suppressed when coexpressed with Rg2-DC-mC-nuclear localization signals (NLSs), our data strongly suggest that in addition to what is the case for Rx, nuclear hyperaccumulation of GPA2 will block its ability to initiate defense signaling
We found that a forced disequilibrium of the nucleocytoplasmic partitioning of Rx toward nuclear accumulation compromises defense signaling (Figures 7 and 8; see Supplemental Figures 7 and 8 online), showing that a balanced nucleocytoplasmic partitioning is essential for effective Rx-mediated immune signaling
Summary
Innate immunity of plants protects them against pathogens and shares several features with animal innate immunity (Ausubel, 2005). Upon perception of specific pathogenderived virulence proteins, so-called effectors, these immune receptors mediate the induction of a strong defense response. This response is referred to as effector-triggered immunity (ETI) and is often associated with a hypersensitive response (HR), a type of programmed cell death at the infection site (Jones and Dangl, 2006). Plant NB-LRRs share structural and functional similarities with the animal nucleotide binding leucine-rich repeat (NLR) family of innate immune receptors (Ye and Ting, 2008) and the metazoan apoptosis factors Apaf-1 and CED-4, which are all classified as STAND Other NB-LRRs are thought to act as guards that sense perturbations caused by their cognate effectors of specific host proteins, called guardees, virulence targets, decoys, or baits (Van der Biezen and Jones, 1998a; van der Hoorn and Kamoun, 2008; Collier and Moffett, 2009), which are often bound to the N terminus of NB-LRRs (Collier and Moffett, 2009; Lukasik and Takken, 2009)
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