Mapping Winterhardiness in Garden Roses

Abstract

Field winterhardiness is a critical trait in rose cultivars (Rosa ×hybrida) grown in northern climates. Although the molecular basis of cold hardiness has been well documented in model organisms such as Arabidopsis thaliana, little is known about the genetics and mechanisms underlying winterhardiness in roses. This research aims to explore the genetic control of winterhardiness for application in breeding programs using quantitative trail loci (QTL) analysis in two biparental rose populations derived from cold-hardy roses of the Canadian Explorer Series Collection. Field winterhardiness was assessed as a complex trait with winter damage and regrowth recorded in multiyear and multilocation trials in Ontario and Saskatchewan, Canada. In addition, this research explored the relationship between field measurements and electrolyte leakage recorded under artificial conditions. Electrolyte leakage had limited utility for application in rose breeding programs as a substitute for field evaluation, but did enable identification of QTL associated with potential cold hardiness candidate genes. A QTL for electrolyte leakage mapped to a genomic region that harbors a CBF1-like transcription factor. A total of 14 QTLs associated with field winter damage and regrowth were discovered, and they explained between 11% and 37% of the observed phenotypic variance. Two QTL associated with winter damage and regrowth overlapped with a known QTL for black spot (Diplocarpon rosae) disease resistance, Rdr1, in an environment under high disease pressure. Due to the complexity of field winterhardiness and its direct reliance on intertwined factors, such as overall plant health, moisture status, snow cover, and period of prolonged sub-zero temperatures, field trials are the ultimate measurement of field winterhardiness. Transgressive segregation was observed for all traits, and it was most likely due to complementary gene action. Field winter damage and regrowth were highly heritable in single environments, but they were subject to genotype × environment interaction resulting from pest pressure and severe climatic conditions.