1 September 2002 Giant foxtail (Setaria faberi) outcrossing and inheritance of resistance to acetyl-coenzyme A carboxylase inhibitors
Dean S. Volenberg, David E. Stoltenberg
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Gene flow via pollen and inheritance of acetyl-coenzyme A carboxylase (ACCase) inhibitor resistance in giant foxtail have not been previously characterized. Therefore, experiments were conducted to quantify outcrossing rates and flowering periods of giant foxtail accessions resistant or susceptible to ACCase inhibitors and to determine the inheritance pattern of gene(s) that confer resistance. In greenhouse experiments, outcrossing rates between resistant and susceptible parents ranged from 0.24 to 0.73%, as gauged by the response of F1 plants to fluazifop-P. Resistant plants and susceptible plants flowered at similar times, with peak flowering occurring 63 to 67 d after planting. During this period, flower initiation was nearly twice as great for resistant plants as for susceptible plants. In inheritance experiments F2 plants segregated in a 1:2:1 ratio of resistant–intermediate–susceptible phenotypes after exposure to fluazifop-P, indicating that resistance was associated with a single nuclear, incompletely dominant allele. The very low rates of outcrossing among giant foxtail plants in the greenhouse indicate that gene flow of resistance traits in the field is likely to occur primarily by seed immigration rather than by pollen movement. However, gene flow of herbicide resistance traits via pollen provides a mechanism in which multiple resistance may develop among giant foxtail populations that are resistant to other classes of herbicides.

Nomenclature: Fluazifop-P; giant foxtail, Setaria faberi Herrm. SETFA.

Dean S. Volenberg and David E. Stoltenberg "Giant foxtail (Setaria faberi) outcrossing and inheritance of resistance to acetyl-coenzyme A carboxylase inhibitors," Weed Science 50(5), 622-627, (1 September 2002). https://doi.org/10.1614/0043-1745(2002)050[0622:GFSFOA]2.0.CO;2
Received: 26 November 2001; Accepted: 12 April 2002; Published: 1 September 2002
gene flow
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