Genetic mapping and validation of QTLs associated with resistance to Calonectria leaf blight caused by Calonectria pteridis in Eucalyptus

• Autor(a) principal: Zarpelon, Talyta Gafassi
• Data de Publicação: 2014
• Outros Autores: Guimarães, Lúcio Mauro da Silva, Faria, Danielle Assis, Coutinho, Marcelo Magalhães, Cápua Neto, Braz, Teixeira, Ramon Ubirajara, Grattapaglia, Dario, Alfenas, Acelino Couto
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: LOCUS Repositório Institucional da UFV
• Texto Completo: http://dx.doi.org/10.1007/s11295-014-0803-4; http://www.locus.ufv.br/handle/123456789/22212
• topic: Genetic resistance; Forest pathology; Genetic map; Microsatellite markers

Calonectria leaf blight (CLB) caused by Calonectria pteridis is one of the main leaf diseases in Brazilian Eucalyptus plantations in warm climates with prolonged periods of rain. The main symptoms are leaf spots followed by intense defoliation in highly susceptible plants. Exploiting the existing inter- and intraspecific variability for defoliation is the best option to control this disease. Nevertheless, nothing is known about the genetic architecture of resistance to CLB in Eucalyptus. We built microsatellite-based genetic maps for E. urophylla × E. camaldulensis (EU11 × EC06) F1 family of 89 plants. Four or five clonal replicates per individual offspring were clonally propagated, totalling 445 plants which were phenotyped for defoliation in the basal third of the branches at 30 days following controlled inoculation with a single-spore isolate. Genetic mapping was performed using a pseudo-testcross, and QTLs detected using composite interval mapping. Five QTLs were detected for resistance to CLB; of them, only one could be validated in two unrelated pedigrees, and its effect was conservatively estimated as controlling between 5 and 10 % of the phenotypic variation when the bias derived from the limited size of the mapping population was taken into account. This work provides a starting point for future studies of the genetics of resistance to CLB, and adds further evidence to the challenge of ascertaining the effects of QTLs detected in a single biparental background across unrelated families.