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Palmer amaranth seed longevity
Since it was first identified in 2004, glyphosate-resistant Palmer amaranth has become the most significant weedy pest of cotton in the Southeastern United States. When acceptable control is not realized, and Palmer amaranth is allowed to set seed, population densities can become quite high in infested fields. For example, research conducted by the University of Georgia indicated that Palmer amaranth seed densities exceeded 35,000 seeds per m2 in a cotton field where the glyphosate-resistant biotype had been ineffectively managed.
To combat Palmer amaranth, some cotton growers in Georgia have resumed using pre-plant deep-tillage and in-crop cultivation in fields with high weed population densities. Disturbance activities that redistribute Palmer amaranth seed from the soil surface to depths greater than 1 inch have been shown to reduce the size of the germinable seedbank (Palmer amaranth seeds are extremely small and, generally, don't possess enough energy reserves to foster seedling emergence from deeper than 1 to 2 inches). By reducing the size of the germinable seedbank, we should reduce the number of weeds that can emerge and compete with the crop, and that need to be controlled with post-emergence herbicides. The purpose of this study was to determine how long Palmer amaranth seeds can remain viable following burial.
Glyphosate-resistant and -susceptible Palmer amaranth seed were collected in October of 2007 and 2008. The seed was hand-harvested and -cleaned and divided into replicate seedlots of 100 seed each. Each seedlot was mixed with 3 cubic inches of sand. placed in nylon bags, and buried (in 2009 and 2010) in a Tifton sandy loam at depths ranging from 1/2 inch to 16 inches. Seeds were exhumed at 3 to 6 month intervals for 36 months. Seed viability was determined by counting the number of unearthed seeds that germinated at 86 F over 28 days in a controlled environment.
Initial viability (0 months of burial) of all seedlots was >96% (>96 of 100 seed germinated). There were no differences in viability between the glyphosate-resistant and -susceptible Palmer amaranth seedlots throughout the course of the study. Seed viability was affected by burial duration (viability decreased the longer seeds remained in the soil) and burial depth (seeds that were buried more deeply remained viable for a longer period of time) (Figure 1). After 12 months, seed buried at 1/2, 1, 4 and 16 inches were 44, 48, 53 and 61% viable, respectively. After 24 months of burial, Palmer amaranth viability was 19, 24, 28, and 37% at the 1/2, 1, 4, and 16 inch burial depths, respectively. By 36 months, Palmer amaranth seed viability at 16 inches (22%) was more than double that at 1/2 inch (9%), with 12 and 15% seed viability at 1 and 4 inches, respectively. Results from this study agree with others that were conducted on redroot pigweed (Amaranthus retroflexus) and tall waterhemp (Amaranthus tuberculatus).
Seeds near the soil surface will not be as persistent as those that are buried more deeply. One of the proposed methods of reducing future in-field Palmer amaranth populations is to reposition weed seeds that are near the soil surface to depths that are below the optimal emergence zone through soil inversion (i.e. moldboard plow). The current study suggests that deep burial of Palmer amaranth seeds can mitigate in-field problems in Georgia, but only if the seeds that are present at greater depths have been buried for more than 36 months.
More details about this research can be found in Sosnoskie, L.M., T.M. Webster and A.S. Culpepper. 2013. Glyphosate resistance does not affect Palmer amaranth (Amaranthus palmeri) seedbank longevity. Weed Science. 61:283-288.
Figure 1. The influence of burial duration and depth on the viability of Palmer amaranth seeds. There were no differences between glyphosate-susceptible and glyphosate-resistant populations of Palmer amaranth, therefore data were combined. The entire study was conducted twice in time (2007-2010 and 2008-2011).
Technology for glyphosate-resistant weeds?
A repost today from the Australian Herbicide Resistance Initiative. Int this snap shot, AHRI discusses new Monsanto technology called BioDirect (RNAi) for control of glyphosate-resistant weeds with glyphosate.
I'll admit that I don't know enough about this yet to have much a well-formed opinion on this (and I don't want to muck up the internet with a bunch of inaccurate info - ha!) so I'll just share the text and links below.
Brad
AHRIinsight #2
Do Monsanto have the next big thing?
Imagine if some technology came along that made glyphosate kill glyphosate resistant weeds. If this did happen, what would we do with this technology? BioDirectTM (aka RNAi) is a new concept from Monsanto that could do just that. It could be the next big thing for the herbicide industry.
The ‘i’ in RNAi stands for ‘interference’. RNA is essentially a small piece of genetic code that all living things use to carry out a specific function within a cell, including coding enzymes that plants need to survive. One way of killing the plant is to spray a herbicide that stops a specific enzyme working (this is how most herbicides work). Another way to kill the plant is to knock out the RNA so that the enzyme is not made at all. BioDirectTM involves spraying a combination of herbicide and fragments of RNA that bind to a specific RNA in the plant. The RNA fragments knock out the RNA that codes for resistant enzyme, and the herbicide knocks out any enzyme that is still susceptible to the herbicide.
The initial research into BioDirectTM technology is focused on glyphosate resistant weeds as this is now the biggest challenge facing North American grain growers. However, it may be possible to apply this technology to other herbicides in the future. It is early days, and BioDirectTM will be several years away. At the moment, this technology is very species specific and is also very specific to the exact resistance mechanism that the weed has.
Click here for more detailed information and a video.
CAST issue paper on the threat of herbicide-resistant weeds on soil conservation efforts
I wanted to share a link today to a paper published by CAST, the Council for Agricultural Science and Technology. This paper, entitled "Herbicide-resistant weeds threaten soil conservation gains: finding a balance for soil and farm sustainablity", was released about a year ago and addresses one of the less obvious issues resistance imposes - soil erosion. This paper can be viewed or downloaded (free!) at the link above.
The development and adoption of effective postemergence herbicides, both conventional and GMO-linked, has resulted in tremendous gains in soil conservation for much of the country due to the reduction in "clean" tillage, in-season cultivation to control weeds, and tillage operations to incorporate soil-applied herbicides. This is of particular benefit in regions with summer rain, intense winds, and varied topography (like much of the Midwest where I'm from) but it benefits California growers and citizens too.
I won't attempt (in a Friday afternoon blog post) to repackage the careful assessment and explanation written by Shaw, Culpepper, Owen, Price, and Wilson. I'd encourage you to read through the article for a slightly different view of the complex issues and cost/benefit considerations made by weed managers. In the CAST paper, the issue is largely soil erosion from water but here in California, you might be more likely to consider dust (PM10). I'd offer the point that weed management considerations are full of trade offs - economics, time, environmental; non-chemical weed control efforts are not without problem.
Brad
CAST Abstract. (Shaw et al. 2012)
Tillage has been an integral part of crop production since crops were first cultivated. Growers and scientists have long recognized both beneficial and detrimental aspects of tillage. There is no question that most tillage operations promote soil loss, adversely affect (lower) surface water quality, and negatively impact soil productivity. Weed management is a primary reason for tillage, and until the development of highly effective herbicides, conservation tillage was not feasible. Furthermore, with the development of herbicide-resistant (HR) crops, particularly glyphosate-resistant (GR) crops, herbicides such as glyphosate minimized the need for tillage as a weed control tactic; the resulting crop production systems have been primary enablers for the success of U.S. Department of Agriculture Natural Resource Soil Conservation programs.
Understanding herbicide meachanisms (modes) of action and how they apply to resistance management in orchards and vineyards
Herbicides are defined as a chemical substance that is used to eliminate unwanted plants. This is a very general description and it is important to remember that herbicides differ with respect to when they are used (for example, pre-emergence or post-emergence), their activity (for example, contact or systemic), their selectivity (for example, grasses or broadleaves), and their mechanism of action (also known as: mode of action, site of action). (See this blog post about basic herbicide terminology:http://ucanr.org/blogs/blogcore/postdetail.cfm?postnum=5973)
What is a mechanism of action? The mechanism of action (MOA) is the way the herbicide controls susceptible plants. More specifically, it describes the biological processes that are disrupted by the herbicide. These biochemical pathways control the growth and development of plants; when herbicides are applied, these processes cannot be carried out and plant injury and death will occur.
Where can I find out information about the MOA's? The Weed Science Society of America (WSSA) lists all herbicide MOAs in a downloadable fact sheet. http://www.wssa.net/Weeds/Resistance/WSSA-Mechanism-of-Action.pdf
What do MOAs have to do with herbicide resistance? The over-reliance (across acres and time) on one MOA for weed control in an agricultural system can increase the probability of selecting for an herbicide-resistant population. With repeated applications, susceptible individuals of a target weed species will die off while the numbers of resistant plants will continue to grow. With time, the MOA will no longer control that species in that location. The chances of the population reverting back to a susceptible state are low. To prevent/mitigate herbicide resistance, it is advised to rotate herbicide MOAs to reduce the selective pressure applied by any one product. Note: Several MOAs are comprised of multiple chemical families that are alike with respect to chemical structure and cause similar injury symptoms. Rotating between chemical families within an MOA is not the same as rotating among MOAs.
So, what MOAs do we have available in orchards and vineyards in California?
WSSA Group 1: Inhibition of acetyl CoA carboxylase (ACCase)
What does that mean? These herbicides inhibit the creation of lipids in grasses (broadleaved weeds are usually not affected). Lipids are the principal components of plant cell membranes; if lipid biosynthesis is inhibited, the plant will be unable to produce new plant cells, which are necessary for continued plant growth.
Examples: clethodim (Prism), fluazifop (Fusilade), sethoxydim (Poast)
WSSA Group 2: Inhibition of acetolactate synthase (ALS)
What does that mean? ALS inhibitors stops the production of three amino acids (isoleucine, leucine, and valine), which, in turn stops the production of enzymes and other proteins that are built from these amino acids.
Examples: halosulfuron (Sandea), rimsulfuron (Matrix), penoxsulam (PindarGT)
WSSA Group 3: Inhibition of mitosis
What does that mean? These herbicides inhibit cell division in germinating seedlings and stop lateral root formation. Lateral roots are important for the uptake of water and nutrients from the soil.
Examples: pendimethalin (Prowl H2O), oryzalin (Surflan)
WSSA Group 4: Growth regulators
What does that mean? These herbicides mimic auxin, a naturally produced growth regulator. Although their activity is not completely understood, auxins are known to have roles in cell elongation and cell wall formation, and are known to control lateral growth. Symptoms of their use are distinctive; broadleaved weeds treated with these growth regulators have stems that are often twisted and curled, malformed flowers, thickened or stunted roots, and have cupped, strapped or otherwise deformed leaves.
Examples: 2,4-D
WSSA Groups 5 and 7: Inhibition of photosystem II (PSII)
What does that mean? These herbicides prevent normal transfer of the energy collected from sunlight in the photosynthetic pathway where it is normally used to generate sugars needed for plant growth. Because energy is still being taken in, but is not properly passed along, the now excess energy generates highly reactive free radicals that cause damage to chlorophyll and cell membranes.
Examples: simazine (Princep), diuron (Karmex)
WSSA Group 8: Fatty acid and lipid biosynthesis inhibitors
What does that mean? These herbicides inhibit several plant processes including the synthesis of fatty acids and lipids that may account for reductions in cuticular waxes and the synthesis of proteins, gibberellins and anthocyanins.
Examples: EPTC (EPTAM)
WSSA Group 9: Inhibition of enolpyruvyl shikimate-3-phosphate synthase (EPSPS)
What does that mean? Glyphosate inhibits EPSPS, which stops the production of three aromatic amino acids (tryptophan, phenylalanine, and tyrosine) that are produced through the shikimate pathway. This, in turn, stops the production of enzymes and other proteins that are subsequently built from these amino acids. The shikimate pathway is very important for plant growth; by some estimates, 20% of all carbon fixed in the leaves passes through the shikimate pathway.
Examples: glyphosate (Roundup)
WSSA Group 10: Inhibition of glutamine synthetase
What does that mean? Glutamine synthetase inhibitors stop the conversion of two chemicals, glutamate and ammonia, to glutamine, which allows for an accumulation of ammonia in the plant. Ammonia inhibits photosynthesis and can destroy plant cells.
Examples: glufosinate (Rely 280)
WSSA Group 12: Carotenoid biosynthesis inhibitors
What does that mean? Carotenoids harvest light and transfer the captured energy to chlorophyll molecules. They also have antioxidant properties that help protect chlorophyll from reactive molecules. The absence of carotenoids allows for the destruction of chlorophyll, which is needed for photosynthesis.
Examples: norflurazon (Solicam)
WSSA Group 14: Inhibition of protopophyrinogen oxidase (PPO)
What does that mean? Protoporphyrinogen oxidase (PPO) is an enzyme that catalyzes a biological reaction that is involved in the production of chlorophyll. PPO inhibitors block the production of chlorophyll. More importantly, they cause reactive molecules to form in the cell, which, in turn, destroy existing chlorophyll molecules, carotenoids and destroy cell membranes.
Examples: flumioxazin (Chateau), saflufenacil (Treevix), carfentrazone (Shark), pyraflufen (Venue)
WSSA Group 15: Inhibition of mitosis
What does that mean? These herbicides inhibit the production of very long chain fatty acids and prevent seedlings from developing properly.
Examples: napropamide (Devrinol)
WSSA Groups 20, 21, 29: Cellulose inhibitors
What does that mean? These herbicides inhibit cell wall synthesis; cell walls are necessary for plant growth.
Examples: dichlobenil (Casoron), isoxaben (Trellis), indaziflam (Alion)
WSSA Groups 22: Inhibition of photosystem I (PSI)
What does that mean? These herbicides accept electrons from the photosynthetic pathway that leads to the formation of reactive molecules that destroy lipids, which in turn leads to the breakdown of plant cell membranes.
Examples: paraquat (Gramoxone Inteon), diquat (Diquat)
In general, where can I find out information about a specific herbicide’s MOA? This information is sometimes, but not always, found on the herbicide label. Some manufacturers will directly specify which WSSA group the herbicide belongs to (hypothetical example: Group 9, Glycines), while others will verbally describe the herbicide’s MOA in the product description section of the label (hypothetical example: this product inhibits the enzyme, EPSP synthase). If you are unsure …ASK!
So, if I just rotate my MOAs I’ll be okay, right? If only it were that easy. Rotating chemicals is a start, but there is more to be done than just that. When/if possible: rotate/alternate crops, use certified seed, cultivate, hand-weed, mulch or inter-crop, prevent weeds from going to seed in fields and orchards, prevent weed seed from being dispersed on farm equipment, etc…And remember to scout. Evaluate weed populations both BEFORE and AFTER weed control strategies are employed; this will allow you to detect potentially resistant populations early and manage them most effectively.
NOTE: NOT ALL MOAs ARE AVAILABLE IN ALL CROPS! READ LABELS AND CONSULT PCAs AND FARM ADVISORS BEFORE APPLYING!
This blog is an extension of a previous post: http://ucanr.org/blogs/blogcore/postdetail.cfm?postnum=6404
California Weed Science Society Journal - new issue focused on herbicide resistance!
A quick post today to share a link to the California Weed Science Society Journal. Click here for a direct link to the January 2013 edition of the CWSS Research Update and News. This edition focuses on herbicide resistance and includes articles by UC Farm Advisors, UC Cooperative Extension Specialists, CSU-Fresno faculty, UC Davis researchers, and herbicide industry researchers :
- Introduction - Steve Orloff
- Selection pressure, shifting populations, and herbicide resistance - Lynn Sosnoskie and Brad Hanson
- Implementing methods to avoid weed shifts and weed resistance in Roundup Ready alfalfa systems - Steve Orloff, Dan Putnam, and Mick Canevari
- Herbicide-resistant weed issues and solutions in agronomic crops in the San Joaquin Valley - Steve Wright, Steve Orloff, and Anil Shrestha
- Rotate herbicide modes of action to prevent and manage glyphosate-resistant weeds in orchards and vineyards - Brad Hanson and Lynn Sosnoskie
- Evolution of herbicide-resistant weeds or species shifts in non-crop areas of the Central Valley - Anil Shrestha, Steve Wright, Kurt Hembree, and Rick Miller
- Also, information on the about-to-be-released new book "Weed Control in Natural Areas in the Western United States" - edited by Joe DiTomaso
There will be a number of presentations on herbicide resistance as well as general weed management problems and solutions at the upcoming (Jan 22-25) 65th Annual California Weed Science Society Meeting in Sacramento. The theme this year is "Weed Management: A Career with a Bright Future in California". Click here for a preliminary meeting program.
Take care,
Brad
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