The effect of depth on 1,3,-D concentration was most evident in water seals and bare soil plots. HDPE and VIF plots had more uniform distribution of the fumigant through the soil profile than the water seals plots, especially 48 hours after treatment. However, 1,3-D concentration under the VIF tarp was markedly higher than in all other treatments, which suggests that there could also be differences in the top 5 centimeters of soil. These results imply that the use of a highly impermeable tarp can lead to a more uniform distribution of fumigants in the soil profile and may allow satisfactory pest control with reduced application rates . Soilborne pest control. Pest control data from the 2007 KAC emissions trial and a related 2008 emissions trial were reported previously and are not shown here. In general, however, there were few differences in pest control attributed to the fumigant application shanks used in the trial. Pythium species populations were lower in all treatments than in the untreated control, but no statistical differences were noted in Fusarium species populations among treatments. The high 1,3-D rates and well-prepared soils resulted in complete control of citrus nematodes in the bioassay bags in all treatments and depths. Weed populations were variable among treatments but tended to be lowest in methyl bromide plots and 1,3-D plots sealed with VIF and highest in the water seals and dual 1,3-D application Treatments.Nematodes and soilborne pathogens. All treatments of 1,3-D or methyl bromide effectively controlled citrus nematodes in bio-assay bags buried at 12-, 24- and 36-inch depths in each plot. However, these results, ebb and flow system which were obtained in well-prepared sandy soils with low pest and pathogen populations, may not apply to more challenging field conditions .
Applications of 1,3-D sealed with HDPE or VIF and dual application 1,3-D treatments reduced Fusarium and Pythium species propagules in the soil compared with the untreated plots . These treatments were comparable to methyl bromide in controlling Fusarium and Pythium species. Soil pathogen control with 1,3-D followed by metam sodium and 1,3-D with intermittent water seals was inconsistent between the two experiments, which suggests that specific micro- and macro-level differences in environmental and field conditions may contribute to greater treatment variability and risk to growers. Weed density. When 1,3-D was sealed with HDPE and VIF, broad leaf weed density was reduced to less than 6 weeds per square meter, which was comparable to methyl bromide . These results are similar to a previous nursery study that indicated 1,3-D or 1,3-D plus chloropicrin sealed with HDPE or VIF resulted in weed seed viability and hand-weeding time comparable to methyl bromide . Generally, intermittent water seals after a 1,3-D application resulted in broad leaf weed density similar to the untreated control. Most weeds germinate near the soil surface, thus techniques such as intermittent water seals that limit upward fumigant movement into surface soils can adversely affect weed control. The other surface treatments 1,3-D dual application and 1,3-D followed by metam sodium had intermediate broad leaf weed densities compared to untreated plots and methyl bromide. All fumigation treatments reduced grass weed populations compared to the control plots; however, the greatest reductions were observed in plots treated with methyl bromide, 1,3-D sealed with HDPE or VIF, and 1,3-D followed by metam sodium. It was clear in this study that effective surface treatments can greatly increase weed control with 1,3-D; however, even the best treatments will likely require supplemental weed control to meet grower expectations. Stock vigor and performance. Effects of surface seal treatments and 1,3-D soil fumigation on nursery stock vigor and performance in two nursery trials were evaluated in 2007 to 2010 . In the rose nursery trial, all treatments had similar rootstock vigor and number of marketable plants except when 1,3-D was followed by metam sodium.
During the 2008 growing season, roses grown in plots treated with 1,3-D followed by metam sodium had lower vigor than the other treatments; however, by harvest at the end of the second year, no differences in marketable plants were observed. In the tree nursery trial, tree rootstock vigor was reduced in plots treated with 1,3-D followed by metam sodium and1,3-D with intermittent water seals compared with the other fumigation treatments, but rootstock caliper at the end of the first growing season did not differ among treatments.Compared with some other fumigation-dependent industries, perennial fruit and nut nursery stock production systems face a more difficult transition to methyl bromide alternatives . Despite several years of research, the following significant challenges to widespread adoption of alternatives in the perennial crop nursery industry remain: National and international market expectations for nematode-firee nursery stock limit nursery stock producers to alternatives with very high nematode efficacy at significant depths in the soil. To meet California nursery certification requirements, producers are required to use approved fumigant treatments or conduct a post production inspection. A failed inspection may result in an essentially nonsalable crop. Most alternative treatment schedules are based on the use of 1,3-D , a fumigant that faces its own serious and evolving regulatory issues in California. No currently available alternative fumigant can be used in California to meet certification requirements in nurseries with fine-textured soil at registered rates. Methyl iodide, the alternative fumigant with performance most similar to methyl bromide, is not currently registered in the United States due to a voluntary withdrawal by the manufacturer. Concerns over control of weeds and fungal and bacterial pathogens in the short and long term may further limit adoption of alternatives with a narrower pest control spectrum. Containerized nursery stock production systems are being used in some parts of the industry, but the production costs, market acceptance and long-term viability of this system have not been addressed at the required scale. Adoption of methyl bromide alternatives, where they exist, in the perennial crop nursery industry will ultimately be driven by state and federal regulations and economics. Although it’s heavily regulated, 1,3-D is a viable alternative for growers with coarse-textured soil, but if 1,3-D becomes more difficult to use due to shortages or increasingly stringent regulations, it may be only a short-term solution. No viable fumigant alternatives exist for California nurseries with fine-textured soil, and some of them may be unable to produce certified nursery stock in the absence of methyl bromide. The cost of producing perennial nursery stock using more expensive, laborious or economically risky production methods will ultimately be passed on to customers and could have long-term impacts on the nursery, orchard, vineyard and ornamental industries.Weedy plants can be tolerant of herbicides due to a variety of temporal, spatial, or physiological mechanisms. For instance, a weed may avoid control efforts if it emerges after a burn down herbicide is applied or completes its lifecycle before a postemergence herbicide is applied. Similarly, large-seeded or perennial weeds can emerge from deeper in the soil and may avoid germinating in soil treated with a preemergenceherbicide. Other weedy species have physiological mechanisms of tolerance and avoid control through reduced herbicide uptake or translocation, rapid detoxification, or insensitive target sites. Regardless of the mechanism of tolerance, repeated use of an herbicide can lead to weed shifts in which weed populations become dominated by species that are not affected by the weed control measures used. A classic example of a weed shift in response to herbicides is the change from primarily broad leaf weeds to grass weeds in cereal production after the introduction of the broad leaf herbicide 2,4-D. Weed shifts can also occur following overuse of non-chemical weed control techniques, such as flame weeding or mowing, flood and drain hydroponics that tend to favor populations of grass weeds.Herbicide resistance in weeds is an evolutionary process and is due in large part to selection with repeated use of the same herbicide or products with the same mode of action. Herbicides do not cause resistance; instead, they select for naturally occurring resistance traits. On a population level, organisms occasionally have slight natural mutations in their genetics; some of these are lethal to the individual, some are beneficial, and some are neutral. Occasionally, one of these chance mutations affects the target site of an herbicide such that the herbicide does not affect the new bio-type. Similarly, mutations can affect other plant processes in a way that reduces the plant’s exposure to the herbicide due to reduced uptake or translocation or through more rapid detoxification.
Whatever the cause, under continued selection pressure with the herbicide, resistant plants are not controlled and their progeny can build up in the population . Depending on the initial firequency of the resistance gene in the population, the reproductive ability of the weed, and the competition, it may take several generations until the resistance problem becomes apparent.Two general types of mechanisms confer resistance to herbicides in weeds. Some mechanisms are related to the specific site of action of the herbicide in the plant, and others involve processes not related to the mechanism by which herbicides kill plants; these two types are known as target-site and non-target-site mechanisms, respectively. A certain weed bio-type may be resistant to more than one herbicide. Herbicide cross-resistance occurs when an individual plant is resistant to two different herbicides via the same mechanism of resistance. In this case, resistance is endowed by a single physiological process operating in common for all the herbicides involved. Multiple resistance results from selection by the simultaneous or sequential use of different herbicides, such that resistance to each herbicide is endowed by a different mechanism.Herbicides usually affect plants by disrupting the activity of a specific protein that plays a key role in plant biochemical process. Target-site resistance occurs when the target enzyme becomes less sensitive or insensitive to the herbicide. The loss of sensitivity is usually associated with a mutation in the gene coding for the protein and can lead to conformational changes in the protein’s structure. These physical changes can impair the ability of one or more herbicides to attach to the specific binding site on the enzyme, thus reducing or eliminating herbicidal activity. Although changes in protein structure occasionally result in reduced biological functionality of the enzyme and a related “fitness cost” , many target-site mutations do not have an observable fitness cost. Certain herbicide groups are particularly vulnerable to developing target-site resistance, because resistance can be endowed by several mutations, thus increasing the probability of finding resistant mutants in weed populations— even in those not previously exposed to that herbicide group. For example, specific mutations resulting in seven different amino acid substitutions in the acetolactate synthase gene are known to confer resistance to ALS-inhibiting herbicides in weed bio-types selected under field conditions. Something similar occurs with the grass herbicides that inhibit the enzyme acetyl coenzyme A carboxylase . In these cases, at least five point mutations are associated with cross-resistance patterns. These can be observed at the whole plant level and involve four classes of ACCase-inhibiting herbicides. The existence of so many mutations conferring resistance is the reason that resistance to these herbicides is firequently found and can evolve rapidly. Several mechanisms confer resistance to herbicides without involving the active site of the herbicide in the plant. Of these, the best known is the case of metabolic resistance due to an enhanced ability to metabolically degrade the herbicide. Non-target-site herbicide resistance has been well demonstrated for several gene families associated with cytochrome P450 monoxidases, glutathione transferases, and glycosyltransferases. Most of these non-target site resistance mechanisms are also present in cultivated plants and are the reason that many herbicides can be used selectively without injuring crops. Non-target-site resistance can evolve from the intensive use of diverse and unrelated selective herbicides that are similarly effective on a certain weed species and share a detoxification pathway or a mechanism precluding their accumulation at the target site that is relatively common in plants. The management of non-targetsite herbicide resistance often represents a greater challenge than management of target-site resistance, because a simple change in herbicide mode of action may not alleviate the problem. Reduced herbicide absorption or translocation can contribute to resistance in certain bio-types. These have generally been accessory mechanisms that contribute toward resistance in addition to major resistance mechanisms. However, recent evidence suggests that changes in absorption or translocation contribute importantly to glyphosate resistance in several weed bio-types.