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Herbicide-resistant biotypes

The term negative cross-resistance is used when a herbicide-resistant biotype is more sensitive to and more easily controlled by classes of herbicides other than the class to which it is resistant. [Pg.127]

In Table 11.2, a listing of known herbicide-resistant biotypes is given according to the type of weeds (dicots and monocots), and herbicide class. [Pg.134]

Table 11.3 gives a listing of the total number of all known herbicide-resistant biotypes in each of the countries where they have been reported. [Pg.134]

Table VIII shows some interesting trends in the first occurrences of herbicide resistant biotypes. Not only are herbicide resistant weeds appearing after fewer repeat annual applications of some of the newer herbicides (e.g., 4 to 5 years of treatment with sulfonylures herbicides), but there seem to be more species that have potential for resistance, as shown by the 26 new cases in 1988. In addition, the resistant biotypes are more fit and competitive than most biotypes resistant to triazine herbicides. Table VIII shows some interesting trends in the first occurrences of herbicide resistant biotypes. Not only are herbicide resistant weeds appearing after fewer repeat annual applications of some of the newer herbicides (e.g., 4 to 5 years of treatment with sulfonylures herbicides), but there seem to be more species that have potential for resistance, as shown by the 26 new cases in 1988. In addition, the resistant biotypes are more fit and competitive than most biotypes resistant to triazine herbicides.
Table VIII. Nuober of States, Provinces and Countries Reporting the First Appearance of Herbicide Resistant Biotypes by Year... Table VIII. Nuober of States, Provinces and Countries Reporting the First Appearance of Herbicide Resistant Biotypes by Year...
Fitness and Ecological Adaptability of Herbicide-Resistant Biotypes... [Pg.419]

It should be possible to assess the potential and the reason for decreased fitness in resistant biotypes in cases where the mechanism of resistance is known (2). Table I lists the herbicides or classes of herbicides to which resistance has been found in field situations and for which the mechanism of resistance is known or suspected. (A complete list of weeds with herbicide resistant biotypes as of December, 1988 is presented in the chapter by LeBaron and McFarland in this book.)... [Pg.421]

In March 2006 the International Survey of Herbicide-Resistant Weeds recorded 305 herbicide-resistant biotypes with 182 weed species - 109 dicotyledonous and 73 monocotyledonous weeds [1]. The relatively steady increase in the number of new cases of resistance since 1980 accounts for the increasing importance of herbicide resistance in weeds in the major agricultural regions (Fig. 1.1). [Pg.5]

Zeng, L. and Baird, W. V. (1997). Genetic basis of dinitroaniline herbicide resistance in a highly resistant biotype of goosegrass (Eleusine indica). J. Hered. 88, 427-432. [Pg.262]

Pfister, K. and C.J. Amtzen (1979). The mode of action of photosystem II-specific inhibitors in herbicide-resistant weed biotypes. Z. Naturforsch. Sect. C Biosci., 34 996-1009. [Pg.109]

Triazines were one of the first family of herbicides where weed resistance was widely recognized and documented in the literature. A simazine-resistant biotype of common groundsel was identified in Washington, United States, in 1968. Since then biotypes of at least 66 triazine-resistant weed species have been reported, mostly in the United States, Canada, and Europe (Heap, 2006). [Pg.111]

Masabni et al (1996) identified a Ser264 to Thr (threonine) mutation in a resistant biotype of common purslane. This conferred a high level of resistance to atrazine and also to linuron, a substituted urea herbicide. This was the first report of a Ser264 to Thr substitution in higher plants selected under field conditions. Previously, this mutation had only been selected through tissue culture in tobacco and potato (Sigematsu et al, 1989 Smeda etal, 1993). [Pg.115]

In contrast, Ernst et al, (1996) have shown that a substitution at Ser264 does not necessarily lead to herbicide resistance. They found both Ser and Gly at position 264 in various sensitive and resistant biotypes of common groundsel. However, all resistant biotypes of black nightshade had Gly at position 264, but some of the sensitive biotypes also had Gly at this position. They suggested that the effect of this mutation in sensitive biotypes was overcome by two additional mutations in these biotypes alanine at position 251 (Ala25i) to arginine (Arg) and valine at position 280 (Val280) to leucine (Leu). In sensitive common lambsquarters, only Ser was present at position 264 either Ser or Gly were detected at position 264 in different atrazine-resistant plants (Ernst et al, 1996). [Pg.115]

In other weed biotypes, resistance to triazine herbicides is likely conferred by rapid metabolism of the herbicides to inactive compounds. A chlorotoluron-resistant biotype of blackgrass (slender foxtail) was cross-resistant to various other groups of herbicides, including triazines (Kemp et al., 1990). The mechanism of chlorotoluron resistance was Cyt P450-based enhanced oxidative metabolism through /V-demethylation and ring-methyl hydroxylation (Moss and Cussans, 1991). Consequently, it is likely that resistance to triazines in this blackgrass biotype is also due to enhanced herbicide detoxification. [Pg.116]

The high efficacy of triazine herbicides and their repetitive use in crops and noncrop situations has resulted in the selection of weeds that are resistant to these herbicides or are not well controlled at the lower rates now being used. In most instances, triazine resistance is due to an alteration in the herbicide-binding site in PS II. Despite the widespread occurrence of triazine resistance, these herbicides are still widely used, even in fields in which triazine-resistant biotypes are known to occur. The rate of increase in the selection for triazine-resistant weed species depends in part on the integration of alternative weed control strategies, in addition to the use of triazine herbicides, for control of these weed species. Due to their resistance mechanism, many triazine-resistant weeds are less competitive than their susceptible counterparts. [Pg.116]

Fuerst, E.P., C.J. Arntzen, K. Pfister, and D. Penner (1986). Herbicide cross-resistance in triazine-resistant biotypes of four species. Weed Sci., 34 344-353. [Pg.117]

Soon after the discovery of triazine-resistant common groundsel, another equally important discovery was made. Radosevich and DeVilliers (1976) found that the mechanism of resistance in this weed was due to insensitive chloro-plasts that were capable of photosynthesis, even in the presence of simazine or atrazine. This was surprising because earlier research had confirmed that there were no differences in plant selectivity or susceptibility due to the origin of chloroplasts. Moreland (1969) had reported that isolated chloroplasts were equally inhibited to simazine whether they came from tolerant com or susceptible spinach. Radosevich and Appleby (1973) had confirmed there were no differences between the susceptible and resistant biotypes of common groundsel due to herbicide uptake, distribution, or metabolism, whereas it is known that com metabolizes triazine herbicides (Shimabukuro, 1985). [Pg.120]

The levels of infestations or seriousness of triazine resistance within each species varies gready. The author is aware of 19 cases where the resistant weed is no longer present or cannot be identified as resistant to triazine herbicides. In other cases, the current status is unknown. Several triazine-resistant biotypes are likely to be of little or no agronomic importance within a geographical area. [Pg.123]

In some cases, even before a weed is confirmed in laboratory tests to be resistant to an herbicide, the farmer has already changed his weed control program and the resistant weed may no longer be easy to find. There have been also cases where the resistant weed was identified as one species, but was later confirmed by a taxonomist as another. In those cases where no qualified weed scientist was available to conduct confirmation tests, the resistant biotypes are not listed as resistant, even though they may no longer be controlled with the once effective herbicide. [Pg.123]

Until the mid-1990s, multiple-resistance (i.e., resistance to more than one herbicide mode of action within the same biotype) had not been reported within North America. However, Foes et al. (1996) found a kochia biotype from western Illinois resistant to atrazine and several ALS-inhibiting herbicides. Lopez-Martinez et al. (1996) reported that a triazine-resistant Echinochloa species found in atrazine-treated com also showed cross-resistance to quinclorac. Clay and Underwood (1989) and Clay (1989) reported that one triazine-resistant biotype of American willowherb was also resistant to paraquat from a hop garden in the United Kingdom treated annually for 25 years with simazine and paraquat. [Pg.127]

Excellent progress has been made in the understanding of the cause, nature, genetics, mechanism and solutions of herbicide-resistant weeds since the first triazine-resistant common groundsel was reported more than 35 years ago. Resistance management programs have been extremely successful in controlling most weeds that have developed resistance to the triazine herbicides. However, research is critical to better understand the rapid increase and spread of many new weed biotypes resistant to several classes of herbicides. [Pg.128]


See other pages where Herbicide-resistant biotypes is mentioned: [Pg.140]    [Pg.421]    [Pg.423]    [Pg.425]    [Pg.427]    [Pg.429]    [Pg.169]    [Pg.140]    [Pg.421]    [Pg.423]    [Pg.425]    [Pg.427]    [Pg.429]    [Pg.169]    [Pg.490]    [Pg.7]    [Pg.67]    [Pg.67]    [Pg.115]    [Pg.115]    [Pg.116]    [Pg.119]    [Pg.120]    [Pg.123]    [Pg.124]    [Pg.125]    [Pg.126]    [Pg.126]    [Pg.127]    [Pg.127]    [Pg.128]   
See also in sourсe #XX -- [ Pg.440 , Pg.441 ]




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