Abstract

ABSTRACT Necrotic lesions and vein necrosis characteristic of the hypersensitive response (HR) controlled by the dominant resistance gene Ny develop in potato cv. Pito after infection with potato virus Y ordinary strain (PVY masculine) at a low temperature (16/18 degrees C night/day). In contrast, at high temperatures (19/24 degrees C night/day), large coalesced lesions develop in the lower infected leaves, which wither and remain hanging from stems forming the leaf-drop symptom; mosaic symptoms with no necrosis also develop in the top leaves. The genetic basis of the leaf-drop symptom and its dependence on temperature were examined using a novel approach involving 58 haploids (2n = 24) derived from 'Pito' (2n = 48) through anther culture. These haploids and 'Pito' were graft-inoculated with PVY(O) at 19/24 to 25 degrees C (night/day). Necrotic symptoms were expressed in 28 haploids, of which 18 haploids (phenotype class N) developed top necrosis, vein necrosis, or both and necrotic lesions that are characteristic of HR. Ten haploids showed leaf drop similar to 'Pito' (phenotype class LD). Thirty haploids were susceptible and showed only mosaic symptoms (phenotype class S). These data indicated that necrosis was induced by a single dominant gene, Ny, in the simplex condition. However, the three distinct phenotypic classes (N, LD, and S) among the haploids grown under the same environmental conditions showed that another locus (gene) was involved in modifying the HR triggered by Ny. Data suggested that this locus contains a dominant temperature-dependent modifier (Tdm) gene that alters the expression of PVY-induced HR at higher temperatures, resulting in leaf drop.

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