Utilization of a major brown rust resistance gene in sugarcane breeding

Brown rust, caused by Puccinia melanocephala, has had devastating effects on sugarcane (Saccharum spp.) breeding programs and commercial production. The discovery of Bru1, a major gene conferring resistance to brown rust, represented a substantial breakthrough. Markers for Bru1 are the first available for sugarcane molecular breeding. The contribution of Bru1 towards brown rust resistance in the Canal Point (CP) sugarcane breeding program was determined as a means of directing future breeding strategies. Bru1 was detected in 285 of 1,072 (27 %) clones used for crossing; this germplasm represents the genetic base for cultivar development in Florida. The frequency of Bru1 was greatest in CP clones (42 %) and lowest among Louisiana clones (6 %). Bru1 was not detected in clones with year assignments before 1953. However, Bru1 frequency increased from 15 % (assignments 1975-1985) to 47 % in the current decade. The increase coincided with the introduction of brown rust to Florida. Bru1 was detected in 155 (32 %) of 485 parental clones tested for brown rust susceptibility at two field locations. Of clones classed resistant to brown rust, 154 (59 %) contained Bru1, yet none of 100 susceptible clones contained the gene. Bru1 was detected in 667 (44 %) clones in the second clonal stage of selection, 87 % of which were free of brown rust symptoms. Bru1 is the predominant source of resistance in the Florida sugarcane genetic base. Efforts to identify and integrate new brown rust resistance genes must be pursued to minimize risks associated with a future breakdown in major gene resistance provided by Bru1.

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Bibliographic Details
Main Authors: Glynn, Neil C., Laborde, Chris, Davidson, R. Wayne, Irey, Mike S., Glaz, Barry, D'Hont, Angélique, Comstock, Jack C.
Format: article biblioteca
Language:eng
Subjects:F30 - Génétique et amélioration des plantes, H20 - Maladies des plantes, Saccharum officinarum, Puccinia melanocephala, rouille, amélioration des plantes, gène, résistance génétique, génétique moléculaire, marqueur génétique, http://aims.fao.org/aos/agrovoc/c_6727, http://aims.fao.org/aos/agrovoc/c_27331, http://aims.fao.org/aos/agrovoc/c_6710, http://aims.fao.org/aos/agrovoc/c_5956, http://aims.fao.org/aos/agrovoc/c_3214, http://aims.fao.org/aos/agrovoc/c_35130, http://aims.fao.org/aos/agrovoc/c_27577, http://aims.fao.org/aos/agrovoc/c_24030, http://aims.fao.org/aos/agrovoc/c_2985,
Online Access:http://agritrop.cirad.fr/567461/
http://agritrop.cirad.fr/567461/1/document_567461.pdf
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Summary:Brown rust, caused by Puccinia melanocephala, has had devastating effects on sugarcane (Saccharum spp.) breeding programs and commercial production. The discovery of Bru1, a major gene conferring resistance to brown rust, represented a substantial breakthrough. Markers for Bru1 are the first available for sugarcane molecular breeding. The contribution of Bru1 towards brown rust resistance in the Canal Point (CP) sugarcane breeding program was determined as a means of directing future breeding strategies. Bru1 was detected in 285 of 1,072 (27 %) clones used for crossing; this germplasm represents the genetic base for cultivar development in Florida. The frequency of Bru1 was greatest in CP clones (42 %) and lowest among Louisiana clones (6 %). Bru1 was not detected in clones with year assignments before 1953. However, Bru1 frequency increased from 15 % (assignments 1975-1985) to 47 % in the current decade. The increase coincided with the introduction of brown rust to Florida. Bru1 was detected in 155 (32 %) of 485 parental clones tested for brown rust susceptibility at two field locations. Of clones classed resistant to brown rust, 154 (59 %) contained Bru1, yet none of 100 susceptible clones contained the gene. Bru1 was detected in 667 (44 %) clones in the second clonal stage of selection, 87 % of which were free of brown rust symptoms. Bru1 is the predominant source of resistance in the Florida sugarcane genetic base. Efforts to identify and integrate new brown rust resistance genes must be pursued to minimize risks associated with a future breakdown in major gene resistance provided by Bru1.