CONICET | Buscador de Institutos y Recursos Humanos

Sugarcane brown rust, caused by Puccinia melanocephala, is a severe foliar disease that takes place in almost all countries where sugarcane is grown. Resistant cultivars development is the main control strategy for brown rust due to its efficiency and sustainability. Furthermore, diversification of varieties is considered a key to successfully controlling rust as this will reduce the impact of the disease. Because of these, the Programa de Mejoramiento Genético de la Caña de Azúcar of the Estación Experimental Agroindustrial Obispo Colombres invest in the development of resistant cultivars. The aim of this work was to identify genomic regions associated with a brown rust resistance source in sugarcane, different from the well-known resistant gene Bru1. A Selective Genotyping approach was carried out with an F1 progeny of 300 clones obtained from a cross between TUC 00-36 and RA 87-3, highly susceptible and highly resistant to brown rust, respectively. Both cultivar were found to be Bru1 negative. A total of 60 out of the 300 clones were selected according to their reactions to brown rust. The selected population was tested for brown rust reactions under natural infection in field during two crop seasons and under artificial infection in greenhouse. Whole-genome profiling of the population and their progenitors were obtained by DArTSeq technology. Field evaluations showed that 35 clones were rated as resistant and 25 clones as susceptible. Under controlled conditions, 33 clones were rated as resistant and 27 as susceptible to the disease. From the DArTSeq genotyping technology a total of 23,299 SNP markers (Single Nucleotide Polymorphism) were obtained. The SNPs were cleaned and filtered. A total of 8,625 SNPs were included in the single marker analysis and 48 markers linked significantly to the brown rust resistant trait. To validate the linkage observed, a multiple regression analysis was done and identified 34 SNPs significantly linked to resistance alleles in both infection conditions, explaining 42% to 65% of phenotypic variability observed,. These markers loci would contribute for molecular-marker-assisted breeding, enabling a more accurate and reliable selection of resistant clones carrying the novel resistance sources, even in absence of the disease. Moreover, the expansion of the genetic bases of brown rust resistance will diverse the resistance sources in field increasing its durability.

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