Managing the risks of herbicide resistance in wild oat

被引:5
作者
Cavan, G [1 ]
Cussans, J [1 ]
Moss, S [1 ]
机构
[1] IACR Rothamsted, Dept Crop & Weed Sci, Harpenden AL5 2JQ, Herts, England
关键词
wad oat; Avena fatua L. AVEFA; aryloxyphenoxypropionate herbicide; cyclohexanedione herbicide; model; weed life cycle; ACCase inhibitor; evolution; cultural control; rotation; AVEFA;
D O I
10.1614/0043-1745(2001)049[0236:MTROHR]2.0.CO;2
中图分类号
S3 [农学(农艺学)];
学科分类号
0901 [作物学];
摘要
A single dominant mutation conferring resistance to aryloxyphenoxyprop ion ate (AOPP) and cyclohexanedione (CHD) herbicides was incorporated into a quantitative model for the population development of wild oat. The model was used to predict the times required to develop field resistance in a number of different scenarios. Field resistance was defined as a threshold of four plants m(-2) surviving herbicide treatment, and in most scenarios, a very large proportion of these plants were resistant. The model predicts that plow cultivation could delay the development of resistance relative to tine cultivation. With an initial seed bank of 100 Seeds m(-2) and annual use of AOPP/CHD herbicides, which kill 90% of susceptible but no resistant plants, field resistance develops in 15 yr with annual tine cultivation 10 cm deep but only after 23 yr with annual plowing 20 cm deep. The model predicts that herbicide rotation can dramatically increase the times required for field resistance to develop in a tine cultivation system. With annual use of AOPP/CHD herbicides, field resistance develops in 15 yr, whereas using alternative modes of action 1 in 2 yr delays field resistance to 28 yr. The model predicts that resistance can be delayed for at least 66 yr if three herbicides, each with a different mode of action, are rotated and each herbicide causes 90% mortality. The model predictions on the number of years required for field resistance to develop are not highly sensitive to the initial density of the seed bank (range modeled = 10(2) to 10(4), the mutation rate for resistance (10(-4) to 10(-7) per generation), the rate of outcrossing (0.1 to 100%) or the herbicide kill rare (80 to 95%).
引用
收藏
页码:236 / 240
页数:5
相关论文
共 25 条
[1]
[Anonymous], 1976, WILD OATS WORLD AGR
[2]
Mapping risk areas for resistance to ACCase inhibitor herbicides in Manitoba [J].
Bourgeois, L ;
Morrison, IN .
CANADIAN JOURNAL OF PLANT SCIENCE, 1997, 77 (01) :173-179
[3]
Cocker KM, 2000, WEED RES, V40, P323, DOI 10.1046/j.1365-3180.2000.00192.x
[4]
Cousens R. D., 1986, Proceedings, EWRS symposium on economic weed control., P269
[5]
DERRICK RA, 1933, SCI AGR, V13, P458
[6]
A revolving dose strategy to delay the evolution of both quantitative vs major monogene resistances to pesticides and drugs [J].
Gardner, SN ;
Gressel, J ;
Mangel, M .
INTERNATIONAL JOURNAL OF PEST MANAGEMENT, 1998, 44 (03) :161-180
[7]
MODELS FOR THE HERBICIDAL CONTROL OF THE SEED BANK OF AVENA-STERILIS - THE EFFECTS OF SPATIAL AND TEMPORAL HETEROGENEITY AND OF DISPERSAL [J].
GONZALEZANDUJAR, JL ;
PERRY, JN .
JOURNAL OF APPLIED ECOLOGY, 1995, 32 (03) :578-587
[8]
Heap IM, 1997, PESTIC SCI, V51, P235, DOI 10.1002/(SICI)1096-9063(199711)51:3&lt
[9]
235::AID-PS649&gt
[10]
3.0.CO