Resistance to quinclorac and ALS-inhibitor herbicides in Galium spurium is conferred by two distinct genes

• Published in: Weed research Vol. 44; no. 5; pp. 355 - 365
• Main Authors: Van Eerd, L.L, McLean, M.D, Stephenson, G.R, Hall, J.C
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.10.2004; Blackwell Science
• Subjects: acetolactate synthase; application rate; auxinic; Biological and medical sciences; enzyme inhibitors; Fundamental and applied biological sciences. Psychology; Galium spurium; genes; genetic resistance; genetics; herbicide resistance; inheritance; inheritance (genetics); multiple-herbicide; Parasitic plants. Weeds; Phytopathology. Animal pests. Plant and forest protection; plant breeding; quinclorac; recessive trait; resistant; sulfonylurea herbicides; thifensulfuron; weed; weed biology; weed control; Oxo-acid-lyases; Resistance; Carbon-carbon lyases; Gene; Enzyme; Weed science; Pesticides; Acetolactate synthase; Enzyme inhibitor; Lyases; Herbicide
• ISSN: 0043-1737; 1365-3180
• DOI: 10.1111/j.1365-3180.2004.00408.x

Summary Classical Mendelian experiments were conducted to determine the genetics and inheritance of quinclorac and acetolactate synthase (ALS)‐inhibitor resistance in a biotype of Galium spurium. Plants were screened with the formulated product of either quinclorac or the ALS‐inhibitor, thifensulfuron, at the field dose of 125 or 6 g active ingredient (a.i.) ha−1 respectively. Segregation in the F2 generation indicated that quinclorac resistance was a single, recessive nuclear trait, based on a 1 : 3 segregation ratio [resistant : susceptible (R : S)]. Resistance to ALS inhibitors was due to a single, dominant nuclear trait, segregating in the F2 generation in a 3 : 1 ratio (R : S). The genetic models were confirmed by herbicide screens of F1 and backcrosses between the F1 and the S parent. F2 plants that survived quinclorac treatment set seed and the resulting F3 progeny were screened with either herbicide. Quinclorac‐treated F3 plants segregated in a 1 : 0 ratio (R : S), hence F2 progenitors were homozygous for quinclorac resistance. In contrast, F3 progeny segregated into three ratios: 1 : 0, 3 : 1 and 0 : 1 (R : S) in response to ALS‐inhibitor treatment. This segregation pattern indicates that their F2 parents were either homozygous or heterozygous for ALS‐inhibitor resistance. Therefore, there were clearly two distinct resistance mechanisms encoded by two genes that were not tightly linked as demonstrated by segregation patterns of the F3.