MOLECULAR AND CELLULAR DYNAMICS INVOLVED IN EFFECTOR RECOGNITION BY THE NEMATODE IMMUNE RECEPTOR GPA2 
A. GOVERSE (1), E. Slootweg (1), H. Overmars (1), J. Roosien (1), O. Caldararu (2), A. Petrescu (2), J. Bakker (1), G. Smant (1) (1) Wageningen University, Netherlands; (2) IBAR, Romania

The potato cyst nematode resistance gene Gpa2 confers resistance to Globodera pallida and is located on a complex locus together with the closely related Potato Virus X (PVX) resistance gene Rx1. They encode NB-LRR immune receptors, which are 88% identical at the amino acid level. Yet, they confer resistance to completely unrelated pathogens. Gpa2 recognizes the secreted nematode effector RBP1, whereas Rx1 detects the PVX coat protein. As many resistance proteins of the NB-LRR class, Gpa2 and Rx1 are predicted to be cytoplasmic because they lack discernable nuclear targeting signals. Previously, we could demonstrate that Rx1 is located both in the cytoplasm and in the nucleus. A similar nucleo-cytoplasmic distribution was observed for Gpa2, although slightly shifted to the cytoplasm. Manipulating the nucleo-cytoplasmic distribution of Gpa2 revealed that both the cytoplasmic and nuclear pool are required for the activation of a cell death response. In addition, we could demonstrate that the recognition of RBP1 takes place in the cytoplasm similar to the recognition of the viral coat protein by Rx1. Evasion of RBP1 recognition by Gpa2 dependents on a single amino acid substitution (S/P), but no difference was observed in the subcellular localisation pattern of Gpa2 activating and non-activating RBP1 variants which reside both in the cytoplasm and nucleus. Computational modeling of the 3D structure suggests that this S/P substitution causes a change in a surface region, which might explain the observed differences in RBP1 recognition by Gpa2. In addition, a structure-informed approach was used to investigate the contribution of other structural motifs present in RBP1 to better understand the underlying mechanisms of RBP1 recognition and activation of Gpa2.

Abstract Number: C24-1
Session Type: Concurrent