<b>HRAC Group 2</b> <font size='2'> (Legacy B) </font> resistant Descurainia sophia from United States, Kansas

International Survey of Herbicide-Resistant Weeds

LOGIN | REGISTER
Saturday, November 23, 2024

HRAC GROUP 2 (LEGACY B) RESISTANT FLIXWEED
(Descurainia sophia)

Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)

United States, Kansas

INTRODUCTION		FLIXWEED
Flixweed (Descurainia sophia) is a dicot weed in the Brassicaceae family. In Kansas this weed first evolved resistance to Group 2 (Legacy B) herbicides in 2006 and infests Winter wheat. Group 2 (Legacy B) herbicides are known as Inhibition of Acetolactate Synthase (Inhibition of Acetolactate Synthase ). Research has shown that these particular biotypes are resistant to chlorsulfuron, imazamox, metsulfuron-methyl, pyroxsulam, sulfosulfuron, triasulfuron, and tribenuron-methyl and they may be cross-resistant to other Group 2 (Legacy B) herbicides. The 'Group' letters/numbers that you see throughout this web site refer to the classification of herbicides by their site of action. To see a full list of herbicides and HRAC herbicide classifications click here.

QUIK STATS (last updated Jan 25, 2011 )
Common Name	Flixweed
Species	Descurainia sophia
Group	Inhibition of Acetolactate Synthase HRAC Group 2 (Legacy B)
Herbicides	chlorsulfuron, imazamox, metsulfuron-methyl, pyroxsulam, sulfosulfuron, triasulfuron, and tribenuron-methyl
Location	United States, Kansas
Year	2006
Situation(s)	Winter wheat
Contributors - (Alphabetically)	Dallas Peterson
Edit this Case \| Add New Case of Resistance \| Add Note

ACADEMIC ASPECTS

Confirmation Tests

Greenhouse, and Laboratory trials comparing a known susceptible Flixweed biotype with this Flixweed biotype have been used to confirm resistance. For further information on the tests conducted please contact the local weed scientists that provided this information.

Genetics

Genetic studies on HRAC Group 2 resistant Flixweed have not been reported to the site. There may be a note below or an article discussing the genetics of this biotype in the Fact Sheets and Other Literature

Mechanism of Resistance

Studies on the mechanism of resistance of Group 2 (Legacy B) resistant Flixweed from Kansas indicate that resistance is due to an altered target site. There may be a note below or an article discussing the mechanism of resistance in the Fact Sheets and Other Literature

Relative Fitness

There is no record of differences in fitness or competitiveness of these resistant biotypes when compared to that of normal susceptible biotypes. If you have any information pertaining to the fitness of Group 2 (Legacy B) resistant Flixweed from Kansas please update the database.

Edit Case | Add Note | Add Article | Add New Case | Help

CONTRIBUTING WEED SCIENTISTS

DALLAS PETERSON

Professor and Extension Weed Specialist Kansas State University Department of Agronomy 3703 Throckmorton Plant Sciences Center 1712 Claflin Road Manhattan, KS 66506-0110, Kansas United States Email Dallas Peterson Web : Web Site Link

ACKNOWLEDGEMENTS
The Herbicide Resistance Action Committee, The Weed Science Society of America, and weed scientists in Kansas have been instrumental in providing you this information. Particular thanks is given to Dallas Peterson for providing detailed information.

Drag a column header and drop it here to group by that column

Herbicide Resistant Flixweed Globally
(Descurainia sophia)

Country

FirstYear

Situation

Active Ingredients

Site of Action

China

2005

Cereals

tribenuron-methyl

Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

China

2011

Winter wheat

MCPA

Auxin Mimics ( HRAC Group 4 (Legacy O)

China

2011

Winter wheat

carfentrazone-ethyl

Inhibition of Protoporphyrinogen Oxidase ( HRAC Group 14 (Legacy E)

United States (Kansas)

2006

Winter wheat

chlorsulfuron, imazamox, metsulfuron-methyl, pyroxsulam, sulfosulfuron, triasulfuron, and tribenuron-methyl

Inhibition of Acetolactate Synthase ( HRAC Group 2 (Legacy B)

Literature about Similar Cases

1 2 3

Page size:

select

Page: of 3

Items 1 to 5 of 12

Deng, W., Q. Yang, Y. Zhang, H. Jiao, Y. Mei, X. Li, and M. Zheng. 2016. Cross-resistance patterns to acetolactate synthase (ALS)-inhibiting herbicides of flixweed (Descurainia sophia L.) conferred by different combinations of ALS isozymes with a Pro-197-Thr mutation or a novel Trp-574-Leu mutation.. Pesticide Biochemistry and Physiology In press : .

Acetolactate synthase (ALS) is the common target of ALS-inhibiting herbicides, and target-site ALS mutations are the main mechanism of resistance to ALS-inhibiting herbicides. In this study, ALS1 and ALS2 genes with full lengths of 2004 bp and 1998 bp respectively were cloned in individual plants of susceptible (S) or resistant (R) flixweed (Descurainia sophia L.) populations. Two ALS mutations of Pro-197-Thr and/or Trp-574-Leu were identified in plants of three R biotypes (HB24, HB30 and HB42). In order to investigate the function of ALS isozymes in ALS-inhibiting herbicide resistance, pHB24 (a Pro-197-Thr mutation in ALS1 and a wild type ALS2), pHB42 (a Trp-574-Leu mutation in ALS1 and a wild type ALS2) and pHB30 (a Trp-574-Leu mutation in ALS1 and a Pro-197-Thr mutation in ALS2) subpopulations individually homozygous for different ALS mutations were generated. Individuals of pHB30 had mutations in each isozyme of ALS and had higher resistance than pHB24 and pHB42 populations containing mutations in only one ALS isozyme. Moreover, the pHB24 had resistance to SU, TP and SCT herbicides, whereas pHB24 and pHB42 had resistance to these classes of herbicides as well as IMI and PTB herbicides. The sensitivity of isolated ALS enzyme to inhibition by herbicides in these populations correlated with whole plant resistance levels. Therefore, reduced ALS sensitivity resulting from the mutations in ALS was responsible for resistance to ALS-inhibiting herbicides in flixweed. Available http://dx.doi.org/10.1016/j.pestbp.2016.08.006..

Xu, X., G. Liu, S. Chen, B. Li, X. Liu, X. Wang, C. Fan, G. Wang, and H. Ni. 2015. Mutation at residue 376 of ALS confers tribenuron-methyl resistance in flixweed (Descurainia sophia) populations from Hebei Province, China.. Pesticide Biochemistry and Physiology 125 : 62 - 68.

The acetolactate synthase (ALS) inhibitor tribenuron has been used continuously for approximately twenty years as an herbicide in winter wheat fields in China. Flixweed (Descurainia sophia) has evolved resistance to tribenuron, due to multiple amino acid mutations at the 197th residue of ALS. In this study, the molecular basis of tribenuron resistance was investigated using two resistant populations, Xingtai (XT) and Shijiazhuang (SJ), and two susceptible populations, Cangzhou (CZ) and Handan (HD). Whole-plant tests and ALS activity assays showed that the two resistant populations were highly resistant to tribenuron. Targeted amplification of ALS genes from the four populations showed that there were two ALS genes in each population, and both of them were expressed in flixweed; the full coding lengths of the two ALS genes were 1998 bp and 2004 bp. Mutations related to tribenuron resistance in flixweed were located in only the 1998 bp paralog. An ALS activity assay showed that the resistant population SJ displayed slight cross-resistance to florasulam, with a resistance factor of 4.81, but the resistant population XT did not have cross-resistance to florasulam. The resistant population XT was found to carry the previously reported mutation Pro197Ser, but the resistant population SJ carried a different mutation, Asp376Glu, known from other weeds but novel in flixweed. Our results demonstrated that multiple versions of ALS genes exist in flixweed and that mutations at multiple sites may result in ALS-inhibitor resistance in this weed..

Deng, W., M. J. Liu, Q. Yang, Y. Mei, X. F. Li, and M. Q. Zheng.. 2015. Tribenuron-methyl resistance and mutation diversity of Pro197 in flixweed (Descurainia Sophia L.) accessions from China.. Pesticide Biochemistry and Physiology 117 : 68 - 74.

Flixweed (Descurainia Sophia L.) is a problematic weed in winter wheat fields in China, which causes great loss of wheat yield. A total of 46 flixweed accessions from winter wheat-planting areas were collected and used for the survey of resistance to tribenuron-methyl and Pro197 mutation diversity. According to the “R” resistance rating system, 16 flixweed accessions have evolved resistance to tribenuron-methyl, 13 accessions have high risk of developing resistance to this herbicide and 17 accessions are susceptible. The mutation of Pro197 codon (CCT) changed proline (Pro) into leucine (Leu) (homozygous, RR), serine (Ser, RR), histidine (His, RR), threonine (Thr, RR), Pro/Leu (heterozygous, RS), Pro/Ser (RS), Pro/His, Pro/Thr (RS) and Pro/Tyr (RS). Among these amino acid changes, a Pro197-Pro/Tyr (heterozygous, RS) substitution caused by the mutation of two successive nucleotides was identified for the first time in resistant weed species. In addition, the Pro197-His and Pro197-Pro/His mutations have not been reported previously in flixweed. Finally, a CPAS marker was developed to identify flixweed plants with or without Pro197 mutation..

Han XueJing ; Dong Yi ; Sun XiaoNa ; Li XueFeng ; Zheng MingQi. 2012. Molecular basis of resistance to tribenuron-methyl in Descurainia sophia (L.) populations from China. Pesticide Biochemistry and Physiology 104 : 77 - 81.

Two Descurainia Sophia populations, HB16 and HB08, were discovered in China and exhibit high resistance levels to tribenuron-methyl. Resistance ratio values of HB16 and HB08 were 153.47 and 651.20, respectively. The extractable acetohydroxy acid synthase (AHAS) activity was similar between resistant and susceptible populations. However, AHAS from HB16 and HB08 was less sensitive to inhibition of tribenuron-methyl comparing to susceptible population. The tribenuron-methyl I₅₀ values for HB16 and HB08 were 46.25 and 54.07 greater than that for susceptible population respectively. Pro-197-Ser and Pro-197-Leu mutations were identified in AHAS extracted from HB16 and HB08 plants respectively. AHAS insensitivity of resistant D. Sophia caused by Pro197 mutation could be responsible for high resistance to tribenuron-methyl..

Cui HaiLan ; Zhang ChaoXian ; Wei ShouHui ; Zhang HongJun ; Li XiangJu ; Zhang YanQiu ; Wang GuiQi. 2011. Acetolactate synthase gene proline (197) mutations confer tribenuron-methyl resistance in flixweed (Descurainia sophia) populations from China. Weed Science 59 : 376 - 379.

The molecular basis of resistance to tribenuron-methyl, an acetolactate synthase (ALS) - inhibiting herbicide was investigated in four resistant (R) and three susceptible (S) flixweed populations. The resistance level in the R populations was assessed in whole-plant pot experiments in a greenhouse, and resistance indices ranged from 723 to 1422. The ALS genes of the three S populations and four R populations were cloned and sequenced, and the full coding sequence of the ALS gene of flixweed was 2,004 bp. The sequences of the ALS genes of the three S populations collected from Shaanxi, Gansu, and Tianjin were identical. Comparison of the ALS gene sequences of the S and R populations with Arabidopsis revealed that proline at position 197 of the ALS gene was substituted by leucine in R population SSX-2, by alanine in R population SSX-3, and by serine in R populations TJ-2 and GS-2. In another study of two R flixweed populations from Hebei and Shaanxi, resistance was also related to mutation at position 197 of the ALS gene. Both studies confirmed tribenuron-methyl resistance in flixweed in China, with the resistance mechanism being conferred by specific ALS point mutations at amino acid position 197..

1 2 3

Page size:

select

Page: of 3

Items 1 to 5 of 12

PERMISSION MUST BE OBTAINED FIRST if you intend to base a significant portion of a scientific paper on data derived from this site.
Cite this site as: Heap, I. The International Survey of Herbicide Resistant Weeds. Online. Internet. Saturday, November 23, 2024 . Available www.weedscience.org
Copyright © 1993- 2024 WeedScience.org All rights reserved. Fair use of this material is encouraged. Proper citation is requested.