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Glyphosate‐resistant Ambrosia trifida is a competitive and difficult‐to‐control annual broad‐leaved weed in several agronomic crops in the Midwestern United States and Ontario, Canada. The objectives of this study were to compare treatments for control of glyphosate‐resistant A. trifida with tillage followed by pre‐emergence (PRE) and/or post‐emergence (POST) herbicides in glyphosate‐resistant maize and to determine the impact of A. trifida escapes on maize yield. Field experiments were conducted in 2013 and 2014 in grower fields infested with glyphosate‐resistant A. trifida. Tillage prior to maize sowing resulted in 80–85% control compared with no tillage. Tillage followed by PRE application of saflufenacil plus dimethenamid‐P with or without atrazine resulted in 99% control compared with ≤86 and 96% control with PRE herbicides alone at 7 and 21 days after application respectively. Tillage or POST‐only herbicides resulted in 4–14 A. trifida plants m?2, whereas a PRE and POST programme had <3 plants m?2. Maize yield was greatest (13.1–14.2 tonnes ha?1) with tillage followed by PRE and POST herbicide programme. The relationship between maize yield and late‐season density of A. trifida escapes showed a 50% maize yield reduction irrespective of control measures when A. trifida density was 8.4 plants m?2. It was concluded that the combination of tillage with PRE and/or POST herbicides reduced A. trifida density and biomass accumulation early in the season and provided an integrated approach for effective management.  相似文献   
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Recent advances in molecular cytogenetics empower construction of physical maps to illustrate the precise position of genetic loci on the chromosomes. Such maps provide visible information about the position of DNA sequences, including the distribution of repetitive sequences on the chromosomes. This is an important step toward unraveling the genetic mechanisms implicated in chromosomal aberrations (e.g., gene duplication). In response to stress, such as pesticide selection, duplicated genes provide an immediate adaptive advantage to organisms that overcome unfavorable conditions. Although the significance of gene duplication as one of the important events driving genetic diversity has been reported, the precise mechanisms of gene duplication that contribute to pesticide resistance, especially to herbicides, are elusive. With particular reference to pesticide resistance, we discuss the prospects of application of molecular cytogenetic tools to uncover mechanism(s) of gene duplication, and illustrate hypothetical models that predict the evolutionary basis of gene duplication. The cytogenetic basis of duplicated genes, their stability, as well as the magnitude of selection pressure, can determine the dynamics of the genetic locus (loci) conferring pesticide resistance not only at the population level, but also at the individual level. © 2017 Society of Chemical Industry  相似文献   
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BACKGROUND: Auxinic herbicides are widely used for selective control of many broadleaf weeds, e.g. wild mustard. An auxinic‐herbicide‐resistant wild mustard biotype may offer an excellent model system to elucidate the mechanism of action of these herbicides. Classical genetic analyses demonstrate that the wild mustard auxinic herbicide resistance is determined by a single dominant gene. Availability of near‐isogenic lines (NILs) of wild mustard with auxinic herbicide resistance (R) and herbicide susceptibility (S) will help to study the fitness penalty as well as the precise characterization of this gene. RESULTS: Eight generations of backcrosses were performed, and homozygous auxinic‐herbicide‐resistant and auxinic‐herbicide‐susceptible NILs were identified from BC8F3 families. S plants produced significantly more biomass and seed compared with R plants, suggesting that wild mustard auxinic herbicide resistance may result in fitness reduction. It was also found that the serrated margin of the first true leaf was closely linked to auxinic herbicide resistance. Using the introgressed progeny, molecular markers linked to auxinic herbicide resistance were identified, and a genetic map was constructed. CONCLUSION: The fitness penalty associated with the auxinic herbicide resistance gene may explain the relatively slow occurrence and spread of auxinic‐herbicide‐resistant weeds. The detection of the closely linked markers should hasten the identification and characterization of this gene. Copyright © 2012 Society of Chemical Industry  相似文献   
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Phenoxy herbicides such as 2,4‐dichlorophenoxy acetic acid (2,4‐D) and 4‐chloro‐2‐methylphenoxy acetic acid (MCPA) are selective herbicides used extensively in agriculture for weed control. Wild radish (Raphanus raphanistrum) is a problem weed across the globe and heavily infests crop fields in Australia. Phenoxy herbicides are used to selectively control dicot weeds, including wild radish. As a result of selection, phenoxy‐resistant wild radish populations evolved in Western Australia. In this research, introgression of phenoxy resistance from wild radish to cultivated radish (Raphanus sativus) was investigated following classical breeding procedures. F1 progeny were generated by crossing MCPA‐resistant R. raphanistrum and MCPA‐susceptible R. sativus. F1 hybrids were screened for MCPA resistance. The MCPA‐resistant F1 hybrids were used to produce three generations of backcross progeny. Genetic analyses of F1 and backcross progeny demonstrated introgression of the MCPA‐resistant trait from wild radish to cultivated radish. Implications of phenoxy resistance introgression into cultivated radish include potential development of herbicide‐tolerant radish cultivars or other members of the Brassicaceae family.  相似文献   
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