Clonal evaluation for fusiform rust disease resistance: effects of pathogen virulence and disease escape

Abstract

We evaluated the precision of phenotypic classification for fusiform rust resistance of Pinus taeda L. in a clonally propagated population segregating for the pathotype-specific resistance gene Fr1. In all marker-defined Fr1/fr1 clones screened with low complexity or ambient inoculum, marker–trait cosegregation was complete with no exceptions. Uncommon exceptions (4 of 30) in which marker-defined Fr1/fr1 clones screened with high complexity inoculum were diseased were probably due to a low frequency of spores virulent to Fr1 resistance. Marker–trait cosegregation for fr1/fr1 clones was less reliable, as all ramets of a few clones (5 of 29, 3 of 25, and 4 of 16) remained disease-free with low complexity, high complexity, or ambient inoculum, respectively. We termed disease-free fr1/fr1 ramets “escapes”, since the genetics of the host–pathogen interaction predicted them to be diseased. For nonmarker-defined materials, we considered escapes to be disease-free ramets within clones that had at least one diseased ramet. Narrow-sense heritability estimates for escape rate were 29% and 23% for the low and high complexity inocula, respectively, suggesting that genetic variation in the host is an important component of this resistance mechanism.