Inheritance of multiple herbicide resistance in wild oat (Avena fatua L.)

Abstract

. 2006. Inheritance of multiple herbicide resistance in wild oat (Avena fatua L.). Can. J. Plant Sci. 86: 317-329. To gain some insight into the surprisingly frequent occurrence of multiple herbicide resistant wild oat in western Canada, the inheritance of multiple herbicide resistance was studied in two wild oat (Avena fatua L.) populations, UMWO12-01 and UMWO12-03, from Manitoba, Canada. Both populations are resistant to each of three distinct herbicides, imazamethabenz-methyl, flamprop-methyl, and fenoxaprop-p-ethyl (hereafter referred to as imazamethabenz, flamprop, and fenoxaprop-P, respectively). Crosses were made between each resistant (R) population and a susceptible (S) wild oat population (UM5) (R/S crosses), and between the two resistant populations (R/R crosses). Subsets of parental, F 2 plants, and F 2 -derived F 3 (F 2:3 ) families were treated separately with each of the three herbicides and classified as R or S for individual plants, and homozygous R, segregating, or homozygous S for F 2:3 families. F 2 plants and F 2:3 families from R/S crosses segregated in 3R:1S and 1 homozygous R:2 segregating:1 homozygous S ratios, respectively. These ratios indicate that a single dominant or semi-dominant nuclear gene controls resistance to each of these herbicides in each population. F 2 plants and F 2:3 families from R/R crosses segregated for resistance/susceptibility when treated with either imazamethabenz or flamprop. Therefore, the genes for resistance to these two herbicides are different in each R population. Individual F 2:3 family response demonstrated that the genes were not independent of each other, indicating possible linkage between the genes for resistance to each herbicide. Genetic linkage could explain how the wild oat populations developed multiple resistance in the absence of selection by two of the herbicides, imazamethabenz and flamprop. . Les auteurs ont croisé chaque population résistante (R) avec une population sensible (S) (UM5) (croisements R/S) et les deux populations résistantes entre elles (croisements R/R). Des sous-groupes composés de plants parentaux, de plants de la F 2 et de familles F 3 issues de la F 2 (F 2:3 ) ont été traités séparément avec chacun des trois herbicides, puis chaque plant a été classé R ou S ou R homozygote, ségré-gant ou S homozygote, pour les familles F 2:3 . Les ratios de ségrégation des plants de la F 2 et des familles F 2:3 des croisements R/S s'établissaient respectivement à 3R:1S et à 1 homozygote R :2 ségrégant:1 homozygote S. Ces ratios indiquent qu'un seul gène dominant ou mi-dominant dans le noyau commande la résistance à chaque herbicide au sein de chaque population. Le traitement des plants de la F 2 et des familles F 2:3 des croisements R/R à l'imazaméthabenz ou au flamfrop entraîne la ségrégation pour la résistance/sensibilité. On en conclut que les gènes codant la résistance à ces deux herbicides diffèrent dans chaque population R. La réaction distincte des familles F 2:3 révèle que les gènes ne sont pas indépendants, signe qu'il pourrait...

The Biology of Canadian Weeds. 27.Avena fatuaL. (updated)

“…By the mid-1990s, intergroup-resistant populations Á ACC inhibitor, e.g., fenoxaprop,'ALS inhibitor (group 2), e.g., imazamethabenz,'flamprop (group 25)-resistant populations were confirmed in northwestern Manitoba (Friesen et al 2000). In a study of two such populations, a single dominant or semidominant nuclear gene controlled resistance to each herbicide with possible linkage between the genes (Karlowsky et al 2006).…”

Weed Resistance Monitoring in the Canadian Prairies

“…Eighteen percent of group 1-HR populations exhibited group 2 resistance, even though group 2 herbicides had not been applied frequently in those fields. Linkage between genes for resistance to herbicides of differing site of action or enhanced metabolism may explain how wild oat populations evolved intergroup resistance in the absence of selection by non-group-1 herbicides (Beckie et al 1999b;Karlowsky et al 2006). The distribution and abundance of group 1-HR wild oat reflected past group 1 herbicide use across ecoregions.…”

Non‐target site resistance to flucarbazone, imazamethabenz and pinoxaden is controlled by three linked genes in Avena fatua

“…Furthermore, genes conferring resistance to imazamethabenz and flamprop‐M‐methyl were linked. However, the physiological mechanisms conferring MHR in UMWO12‐01 and UMWO12‐03 are unknown (Karlowsky, ), in contrast to the MHR3 and MHR4 A. fatua populations discussed here. However, as TSR is generally much more prevalent than NTSR (Heap, ), it seems likely that resistance in UMWO12‐01 and UMWO12‐03 is due to TSR.…”

“…Our findings are similar to those of Karlowsky et al . () who investigated the inheritance of MHR in the UMWO12‐01 and UMWO12‐03 Canadian A. fatua populations. They reported that separate single dominant or semi‐dominant nuclear genes conferred resistance to imazamethabenz, flamprop‐M‐methyl and fenoxaprop‐P‐ethyl in both populations.…”

“…For example, for resistance to flucarbazone and pinoxaden, the F 2 families should segregate in the ratio of 9 resistant to both flucarbazone and pinoxaden: 3 resistant to flucarbazone and susceptible to pinoxaden: 3 susceptible to flucarbazone and resistant to pinoxaden: 1 susceptible to both flucarbazone and pinoxaden. For analysis, data from homozygous resistant and segregating families were grouped together to form the resistant category (Karlowsky et al, 2006). Data for the resistance genes for flucarbazone/imazamethabenz and flucarbazone/pinoxaden did not fit this ratio, suggesting that the resistance genes for these herbicides are linked (Table 3).…”