NtTPN1: a RPP8‐like R gene required for Potato virus Y‐induced veinal necrosis in tobacco

Summary Potato virus Y (PVY) is one of the most damaging viruses of tobacco. In particular, aggressive necrotic strains (PVYN) lead to considerable losses in yield. The main source of resistance against PVY is linked to the va locus. However, va‐overcoming PVY isolates inducing necrotic symptoms were observed in several countries. In this context, it is important to find va‐independent protection strategies. In a previous study, the phenotyping of 162 tobacco varieties revealed 10 accessions that do not carry the va allele and do not exhibit typical PVYN‐induced veinal necrosis. Despite the absence of necrotic symptoms, normal viral accumulation in these plants suggests a va‐independent mechanism of tolerance to PVYN‐induced systemic veinal necrosis. Fine mapping of the genetic determinant(s) was performed in a segregating F2 population. The tolerance trait is inherited as a single recessive gene, and allelism tests demonstrated that eight of the 10 tolerant varieties carry the same determinant. Anchoring the linkage map to the tobacco genome physical map allowed the identification of a RPP8‐like R gene, called NtTPN1 (for Nicotiana tabacum Tolerance to PVY‐induced Necrosis1), with the same single‐nucleotide polymorphism in the eight tolerant accessions. Functional assays using homozygous NtTPN1 EMS mutants confirmed the role of NtTPN1 in the tolerance phenotype. PVYN‐induced systemic veinal necrosis in tobacco likely represents an inefficient defense response with hypersensitive response‐like characteristics. The identification of NtTPN1 opens breeding options to minimize the impact of emerging and so far uncontrolled va‐breaking necrotic PVY isolates. Significance Statement PVYN isolates induce systemic veinal necrosis in tobacco leading to considerable yield losses in tobacco crops worldwide. In the current paper, we demonstrate that a RRP8‐like R gene is required for PVYN‐induced systemic veinal necrosis. This is one of a few examples of a disease phenotype due to an active, though inefficient, defense response rather than a direct effect of the viral infection.