Ethylene is not involved in clopyralid action in yellow starthistle (Centaurea solstitialis L.)

Valenzuela-Valenzuela, Juan M; Lownds, Norman K.; Sterling, Tracy M.

doi:10.1016/s0048-3575(02)00003-2

Cited by 9 publications

(11 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mechanism of selective resistance to pyridine herbicides is not due to differential uptake, translocation, or metabolism (Fuerst et al 1996;Valenzuela et al 2001) and currently remains unknown. Upon application of clopyralid or picloram, sensitive biotypes produced more ethylene than resistant types, although this response was not attributed as the major causal factor in conferring resistance in yellow starthistle (Sabba et al 1998;Valenzuela et al 2002) and may instead be a secondary consequence of senescence and lethality in sensitive biotypes (Grossman 2000(Grossman , 2010. It has been postulated that the recessive mutation conferring pyridine-specific resistance in these yellow starthistle biotypes (Sabba et al 2003) may be due to an altered auxin receptor (AFB), similar to that identified in picloram-resistant Arabidopsis mutants (Walsh et al 2006).…”

Section: Mechanisms Of Weed Resistance To Auxinic Herbicidesmentioning

confidence: 99%

Evolution of Resistance to Auxinic Herbicides: Historical Perspectives, Mechanisms of Resistance, and Implications for Broadleaf Weed Management in Agronomic Crops

et al. 2011

View full text Add to dashboard Cite

Auxinic herbicides are widely used for control of broadleaf weeds in cereal crops and turfgrass. These herbicides are structurally similar to the natural plant hormone auxin, and induce several of the same physiological and biochemical responses at low concentrations. After several decades of research to understand the auxin signal transduction pathway, the receptors for auxin binding and resultant biochemical and physiological responses have recently been discovered in plants.However, the precise mode of action for the auxinic herbicides is not completely understood despite their extensive use in agriculture for over six decades. Auxinic herbicide-resistant weed biotypes offer excellent model species for uncovering the mode of action as well as resistance to these compounds. Compared with other herbicide families, the incidence of resistance to auxinic herbicides is relatively low, with only 29 auxinic herbicide-resistant weed species discovered to date. The relatively low incidence of resistance to auxinic herbicides has been attributed to the presence of rare alleles imparting resistance in natural weed populations, the potential for fitness penalties due to mutations conferring resistance in weeds, and the complex mode of action of auxinic herbicides in sensitive dicot plants. This review discusses recent advances in the auxin signal transduction pathway and its relation to auxinic herbicide mode of action. Furthermore, comprehensive information about the genetics and inheritance of auxinic herbicide resistance and case studies examining mechanisms of resistance in auxinic herbicide-resistant broadleaf weed biotypes are provided. Within the context of recent findings pertaining to auxin biology and mechanisms of resistance to auxinic herbicides, agronomic implications of the evolution of resistance to these herbicides are discussed in light of new auxinic herbicide-resistant crops that will be commercialized in the near future.

show abstract

Section: Mechanisms Of Weed Resistance To Auxinic Herbicidesmentioning

confidence: 99%

Evolution of Resistance to Auxinic Herbicides: Historical Perspectives, Mechanisms of Resistance, and Implications for Broadleaf Weed Management in Agronomic Crops

et al. 2011

View full text Add to dashboard Cite

show abstract

“…However, other authors hold that auxin‐induced shoot growth inhibition and herbicide damage are independent of ET because the inhibitor of ET synthesis, aminoethoxyvinyl glycine (AVG), does not prevent leaf epinasty (Keller & Van Volkenburgh ; Valenzuela‐Valenzuela et al . ).…”

Section: Introductionmentioning

confidence: 97%

“…The application of growth inhibiting levels of auxin stimulates ET production, in turn raising levels of ABA, which is considered to be the endogenous growth inhibitor (Grossmann 2000). However, other authors hold that auxin-induced shoot growth inhibition and herbicide damage are independent of ET because the inhibitor of ET synthesis, aminoethoxyvinyl glycine (AVG), does not prevent leaf epinasty (Keller & Van Volkenburgh 1997;Valenzuela-Valenzuela et al 2002). Plants are exposed to a wide range of environmental stress throughout their lives and have developed different mechanisms to increase their tolerance through molecular changes in response to the onset of stress.…”

Section: Introductionmentioning

confidence: 99%

Regulation of epinasty induced by 2,4‐dichlorophenoxyacetic acid in pea and Arabidopsis plants

et al. 2014

View full text Add to dashboard Cite

The herbicide 2,4-dichlorophenoxyacetic acid (2,4-D) causes uncontrolled cell division and malformed growth in plants, giving rise to leaf epinasty and stem curvature. In this study, mechanisms involved in the regulation of leaf epinasty induced by 2,4-D were studied using different chemicals involved in reactive oxygen species (ROS) accumulation (diphenyleniodonium, butylated hydroxyanisole, EDTA, allopurinol), calcium channels (LaCl3), protein phosphorylation (cantharidin, wortmannin) and ethylene emission/perception (aminoethoxyvinyl glycine, AgNO3). The effect of these compounds on the epinasty induced by 2,4-D was analysed in shoots and leaf strips from pea plants. For further insight into the effect of 2,4-D, studies were also made in Arabidopsis mutants deficient in ROS production (rbohD, rbohF, xdh), ethylene (ein 3-1, ctr 1-1, etr 1-1), abscisic acid (aba 3.1), and jasmonic acid (coi 1.1, jar 1.1, opr 3) pathways. The results suggest that ROS production, mainly ·OH, is essential in the development of epinasty triggered by 2,4-D. Epinasty was also found to be regulated by Ca2+, protein phosphorylation and ethylene, although all these factors act downstream of ROS production. The use of Arabidopsis mutants appears to indicate that abscisic and jasmonic acid are not involved in regulating epinasty, although they could be involved in other symptoms induced by 2,4-D.

show abstract

“…Although auxinic herbicides have been used for c. 60 years, their mechanism of action is not fully understood. In some, but not all (Valenzuela‐Valenzuela et al. , 2002), susceptible dicot species, auxinic herbicides induce 1‐aminocyclopropane‐1‐carboxylic acid synthase activity, resulting in increased biosynthesis of ethylene, abscisic acid and ultimately hydrogen peroxide, which leads to cell necrosis (Hansen & Grossmann, 2000; Grossmann et al.…”

Section: Introductionmentioning

confidence: 99%

“…In the aforementioned auxinic herbicide‐resistant biotypes, the mechanism of resistances is hypothesized to be due to altered auxin binding to the target site or altered signal transduction along the auxin pathway (Penuik et al. , 1993; Valenzuela‐Valenzuela et al. , 2001, 2002; Goss & Dyer, 2003).…”

Section: Introductionmentioning

confidence: 99%

Resistance to quinclorac and ALS‐inhibitor herbicides in Galium spurium is conferred by two distinct genes

et al. 2004

View full text Add to dashboard Cite

Summary Classical Mendelian experiments were conducted to determine the genetics and inheritance of quinclorac and acetolactate synthase (ALS)‐inhibitor resistance in a biotype of Galium spurium. Plants were screened with the formulated product of either quinclorac or the ALS‐inhibitor, thifensulfuron, at the field dose of 125 or 6 g active ingredient (a.i.) ha−1 respectively. Segregation in the F2 generation indicated that quinclorac resistance was a single, recessive nuclear trait, based on a 1 : 3 segregation ratio [resistant : susceptible (R : S)]. Resistance to ALS inhibitors was due to a single, dominant nuclear trait, segregating in the F2 generation in a 3 : 1 ratio (R : S). The genetic models were confirmed by herbicide screens of F1 and backcrosses between the F1 and the S parent. F2 plants that survived quinclorac treatment set seed and the resulting F3 progeny were screened with either herbicide. Quinclorac‐treated F3 plants segregated in a 1 : 0 ratio (R : S), hence F2 progenitors were homozygous for quinclorac resistance. In contrast, F3 progeny segregated into three ratios: 1 : 0, 3 : 1 and 0 : 1 (R : S) in response to ALS‐inhibitor treatment. This segregation pattern indicates that their F2 parents were either homozygous or heterozygous for ALS‐inhibitor resistance. Therefore, there were clearly two distinct resistance mechanisms encoded by two genes that were not tightly linked as demonstrated by segregation patterns of the F3.

show abstract

Ethylene is not involved in clopyralid action in yellow starthistle (Centaurea solstitialis L.)

Cited by 9 publications

References 26 publications

Evolution of Resistance to Auxinic Herbicides: Historical Perspectives, Mechanisms of Resistance, and Implications for Broadleaf Weed Management in Agronomic Crops

Evolution of Resistance to Auxinic Herbicides: Historical Perspectives, Mechanisms of Resistance, and Implications for Broadleaf Weed Management in Agronomic Crops

Regulation of epinasty induced by 2,4‐dichlorophenoxyacetic acid in pea and Arabidopsis plants

Resistance to quinclorac and ALS‐inhibitor herbicides in Galium spurium is conferred by two distinct genes

Contact Info

Product

Resources

About