Cellular dynamics underlying Globodera pallida effector RBP-1 recognition and function

One of the most studied effector genes in the field of plant parasitic nematodes is GpRBP-1 from the potato cyst nematode Globodera pallida. This is largely due to the discovery of its matching immune receptor Gpa2 which to date, remains the only matching effector-R gene pair identified for plant-nematode interactions. Although we have gained some understanding of how effector-triggered immunity by Gpa2 depends on the host factor RanGAP2, the cellular mechanisms underlying nematode effector detection by Gpa2 and subsequent activation of plant immune responses remain elusive. Moreover, no knowledge is available about the involvement of RanGAP2-related developmental processes in the subcellular localisation of Gpa2 or GpRBP-1, such as the Ran cycle. The Ran cycle is an energy driven process in which the small GTPase protein Ran is sandwiched between RanGAP2 and RanBP1 to convert to a different energy state, thereby dictating nucleocytoplasmic trafficking. By fusing nuclear and cytoplasmic targeting signals, we demonstrate that the subcellular localisation of the plant immune receptor Gpa2, its nematode effector GpRBP-1, and co-factor RanGAP2 has a precise cellular choreography essential for eliciting a Gpa2-mediated hypersensitive response. Moreover, we show that RanGAP2 inactive mutants have a reduced interaction with GpRBP-1 and that RanGAP2 activity is required for Gpa2-mediated cell death. From our data we present a compelling model wherein GpRBP-1 manipulates the Ran cycle to orchestrate the nucleocytoplasmic trafficking of host cell components, thereby modulating Gpa2-mediated immune responses.