Extensive use of the preemergence herbicide triallate over the last three decades has selected for resistant (R) Avena fatua L. populations in several areas of the United States and Canada. R plants are also cross-resistant to the unrelated pyrazolium herbicide difenzoquat. We made reciprocal crosses between inbred R and susceptible (S) lines to determine the genetic basis of triallate resistance. Seeds from parental lines and F2 populations were treated with soil applications of 0.275, 0.55, or 1.1 kg/ha triallate in the green-house and plant heights recorded after 37 days. Surviving F2 plants were selfed and the resulting F3 families were screened with 1.1 kg/ha triallate. In the F2 populations, assortment of S and R phenotypes fit a 15:1 segregation ratio, suggesting that resistance was controlled by the two independently segregating recessive genes TRR1 and TRR2. None of the 912 F3 progeny from 51 R F2 individuals was susceptible to triallate treatment, further supporting a two-gene mode of inheritance. There was a possible maternal effect on susceptibility at the highest triallate rate tested.
|Original language||English (US)|
|Number of pages||3|
|Journal||Journal of Heredity|
|State||Published - 2002|
Bibliographical noteFunding Information:
From the Department of Plant Sciences and Plant Pathology, Leon Johnson Hall, Montana State University, Bozeman, MT 59717 (Kern, Myers, and Dyer), Department of Land Resources and Environmental Sciences, Montana State University, Bozeman, MT 59717 (Jasien-iuk and Maxwell), and Manitoba Agriculture, Soils and Crops Branch, Box 1149, Carman, MB, Canada R0G 0J0 (Murray). This research was partially supported by the Montana Department of Agriculture, Montana Agricultural Experiment Station, and Monsanto Company. This manuscript has been assigned Journal Series no. 2000-81, Montana Agricultural Experiment Station, Montana State University, Bozeman, MT. Address correspondence to William E. Dyer at the address above, or e-mail: firstname.lastname@example.org.