Herbicide Mode of Action

1. Herbicide Mode of Action Fabián D. Menalled Cropland Weed Specialist Dept. Land Resources and Environmental Sciences Montana State University menalled@montana.edu

2. Why Understand Herbicide Mode of Action? • Better understanding of how herbicides perform • Improve herbicides performance • Diagnosing herbicide injury • Prevent and manage herbicide resistance

3. Some Things to Remember…. • Photosynthesis (food) • Pigments (energy/light capture) • Respiration (energy) • Amino acids (proteins/growth) • Lipids (cell membranes) • Mitosis (cell division)

4. Why do we use herbicides? • Use herbicides to achieve your goal • Reduce the impact of invasive species • Secure the presence of targeted species But not all herbicides are equal!

5. Herbicide Classification - Selectivity - • Selective: controls or suppresses one species of plant without seriously affecting the growth of another plant species • 2,4-D • Nonselective: control plants regardless of species • Roundup

6. Phloem (Roundup) Foliar Contact (Gramoxone) Root Contact (Treflan) Xylem and Phloem (Banvel, Tordon) Xylem (Spike) Site of Absorption and Translocation

7. Mode of Action (Amino Acid Biosynthesis Inhibitors) Site of Action (EPSPS inhibitor) Chemical Family (Glyicines) Active Ingredient (Glyphosate) Commercial Products (Roundup, Durango)

8. Mode of Action • Sequence of events from absorption of the herbicide into the plant until the plant dies

9. Herbicide Mode of Action Absorption Movement Contact Site of Action Toxicity CO2 + H2O Sugar + O2

10. Classification by Mode of Action • Plant Growth Regulators • Amino Acid Biosysthesis Inhibitors • Lipid Biosynthesis Inhibitors • Cell Division Inhibitors • Photosynthesis Inhibitors • Cell Membrane Disrupters • Pigment Inhibitors • Unknown mode of action

11. Plant Growth Regulators • Synthetic auxins (regulate plant growth) • Affect several plant processes such as cell division, cell enlargement, protein synthesis and respiration • Act by upsetting the normal hormonal balance in plants

12. Plant Growth Regulators • Herbicide uptake is primarily through the foliage but root uptake is possible • Translocate in both xylem and phloem • Effective on perennial and annual broadleaf weeds • Selectively kill broadleaf plants • Injury may occur in grasses

13. Examples of PGR

14. More examples of PGR • Transline & Curtail: Clopyralid • Milestone: Amynopiralid • Weedmaster: 2,4-D + Dicamba • Grazon P&D: Triclopyr + Picloran

15. PGR Symptoms • Most obvious on newly developing leaves • Abnormal growth resulting in twisting stems • Stems swelling due to rapid cell division • Leaves on broadleaf plants exhibit cupping, crinkling, strapping, or drawstring affect • Symptoms on grass plants include leaf rolling, crinkling, brace root fusion and malformation. • Flower sterility and missing grain in crops

16. PGR Symptoms Parallel veination due to 2,4-D Photo: HMOA and Crop Injury Symptoms. Univ. of Minnesota Extension

17. PGR Symptoms Leaf cupping caused by dicamba Photo: HMOA and Crop Injury Symptoms. Univ. of Minnesota Extension

18. Photo: Kansas State University Extension Puckered soybeans from Tordon

19. Tordon runoff into soybean field Photo: Kansas State University Extension

20. Growth Regulator Use Concerns • Herbicide resistance • Drift and injury to nontarget plants • Carryover: Tordon • Groundwater Contamination: Tordon

21. Questions, so far?

22. Amino Acid Synthesis Inhibitors • Prevent synthesis of certain amino acids produced by plants but not animals • Excellent foliar and root absorption • Broad weed spectrum • Translocates to shoot and root new growth in both xylem and phloem • Plants stop growing shortly after application • Plant death may be slow (10 days+)

23. Examples of Amino Acid Synthesis Inhibitors

24. More Examples of Amino Acid Synthesis Inhibitors • Amber: Triasulfuron • Cimarron, Escort: Metsulfuron • Journey: Imazapic + glyphosate:

25. Chlorosis of New Growth on Tansy Mustard

26. Plateau Injury Symptoms Stunting Chlorosis of youngest tissue

27. EPSP Inhibitors(Glyphosate) • Tightly adsorbed and inactive in soil • Phloem translocated • Inhibits EPSP enzyme responsible for production of aromatic amino acids phenylalinine, tyrosine and tryptophan • Very nontoxic

28. Gradual Death from Roundup Treatment

29. Glyphosate (Roundup) Injuries chlorosis shortened internodes stem proliferation

30. Roundup on AzaleaYellowing of new growth

31. Strapped leaves on a maple due to glyphosate Mimics 2,4-D and other hormone-like herbicides

32. Questions, so far?

33. Photosynthesis Inhibitors • Control annual or perennial grasses or broadleaves • Shut down the photosynthetic process • Slow starvation of the plant • However, the plant experiences a more rapid death be due to the production of secondary toxic substances • Injury symptoms: yellowing (chlorosis) of leaf tissue followed by death (necrosis) of the tissue

34. Photosynthesis Inhibitors • Controls big sage, shinnery and other oaks, tarbush and creosote bush • Sagebrush thinning and brush sculpting programs • Rangeland, pastures, clearings for wildlife and other non-cropland areas tebuthiuron

35. Photosynthesis Inhibitors • Injury symptoms: • Only occur after the cotyledons and first leaves emerge (do not prevent seedlings from germinating or emerging) • yellowing (chlorosis) of leaf tissue followed by death (necrosis) of the tissue • Older and larger leaves affected first: they take up more of the herbicide-water solution as they are the primary photosynthetic tissue of the plant

36. Injury from PSII herbicide Note the interveinal chlorosis

37. Cell Membrane Disruptor • Postemergence contact herbicides • Little soil activity • Activated by exposure to sunlight to form oxygen compounds such as hydrogen peroxide • These oxygen compounds destroy plant tissue by rupturing plant cell membranes • Perennial weeds usually regrow because there is no herbicide movement to underground root or shoot systems

38. Cell Membrane Disruptor • Controls weeds in just 24 to 48 hours • Broad-spectrum and non-selective control of grasses, broadleaf weeds and sedges • Cheatgrass, kochia, Russian thistle, annual mustards • No residual effect

39. Cell Membrane Disruptor, Injuries Rapid browning (necrosis) of plant tissue

40. Paraquat injury on corn leaves

41. Why Understand Herbicide Mode of Action? • Better understanding of how herbicides perform • Improve herbicides performance • Diagnosing herbicide injury • Prevent and manage herbicide resistance

42. Herbicide Resistance is NOT due to: • Sprayer skips or plugged nozzles • Weather problems that cause poor control 3. Plants that are ‘naturally tolerant’ to the herbicide 4. Genetic changes caused by the herbicide

43. Herbicide Resistance is: The ability of a plant to survive and reproduce after treatment with a dose of herbicide that would normally kill the plant Banvel-resistant kochia

44. Where do Resistant Weeds Come From? It’s all about selection….. One in one million, billion, trillion….?

45. Herbicide Resistance • Selection intensity • Herbicide efficacy • Length of soil residual period • Number of herbicide applications / year

46. Selection Pressure is Affected by: Herbicide Quality “Better” herbicide = more chance of resistance Is herbicide resistance a problem in range and wildlands?

47. Resources • University of Minnesota: • Herbicide Mode of Action and Injury Symptoms(http://www.extension.umn.edu/distribution/cropsystems/DC3832.html) • Kansas State University: • Herbicide Mode of Action • (http://www.oznet.k-state.edu/library/crpsl2/c715.pdf) • Montana State University: • Preventing and Managing Herbicide-resistant Weeds in Montana(http://www.montana.edu/wwwpb/pubs/mt200506.html)

48. Questions?