Effect of Dinitroaniline Herbicides on Plant Resistance to Soilborne Pathogens

Grinstein, A.

doi:10.1094/phyto-66-517

Cited by 28 publications

(9 citation statements)

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“…Even though trifluralin showed no effect on damping-off of cotton seedlings, pendimethalin lowered the effectiveness of fungicides applied in combination with the herbicide (Heydari et al, 2007). In contrast to the results mentioned above, dinitroaniline herbicides may provoke a remarkable increase in resistance of pretreated plants to soil-borne pathogens, such as Fusarium species, even if applied at very low concentrations (Grinstein et al, 1976). Thus, this effect can not surely be attributed to a direct fungitoxic mode of action.…”

Section: Dinitroaniline Herbicidesmentioning

confidence: 62%

Unexpected Side Effects of Herbicides: Modulation of Plant-Pathogen Interactions

Kortekamp¹

2011

Herbicides and Environment

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Section: Dinitroaniline Herbicidesmentioning

confidence: 62%

Unexpected Side Effects of Herbicides: Modulation of Plant-Pathogen Interactions

Kortekamp¹

2011

Herbicides and Environment

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“…The herbicide dinitramine is known to reduce fusarium wilt disease (Grinstein et al, 1976;Cohen et al,, 1986) whilst retarding growth and inducing other morphological changes in treated plants (Ashton & Crafts, 1981). Growth retardation by this dinitroaniline herbicide may be by gibberellin biosynthesis inhibition, a mechanism described by Moreland er al, (1969) for trifluralin, another dinitroaniline herbicide.…”

Section: Discussionmentioning

confidence: 99%

Paclobutrazol and other plant growth‐retarding chemicals increase resistance of melon seedlings to fusarium wilt

et al. 1987

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Studies were made of plant growth retardation and effects on resistanceof melon to fusarium wilt by soil application of paclobutrazol, other ergosterol biosynthesis inhibitors, the fungicide benomyl and the herbicide dinitramine. Paclobutrazol and ancymidol delayed the onset of wilting and were the most effective in reducing wilt incidence. A relationship between effectiveness in retarding seedling elongation and increasing resistance to fusarium wilt was observed. No chemical had a significant effect on pathogen population level in the plant, as determined by stem colonization and direct assessment tests in seedlings grown in soil treated with the chemicals. Excluding benomyl, and to a lesser extent dinitramine, leaf and stem extracts had no inhibitory effect on conidial germination. Gibberellins GA4+7, when applied to seedlings inoculated after germination in paclobutrazol-treated soil nullified growth retardation and increased disease incidence. We suggest that disease incidence reduction by paclobutrazol is due to an effect on piant metabolic processes and not to direct fungitoxicity ofthe compound.

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“…Pretreatment of melon plants with dinitroaniline herbicides markedly increased their resistance to Fusarium wilt (Grinstein et al 1976;Lotan-Pompan et al 2007). Cohen et al (1986) reported that the dinitroaniline herbicides trifluralin and dinitramine were the most effective for inducing resistance to Fom and suggested that reduction of wilt symptoms is associated with a reduction in ethylene production.…”

Section: Epidemiology and Defense Responsesmentioning

confidence: 99%

Breeding melon for resistance to Fusarium wilt: recent developments

et al. 2013

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Melon Fusarium wilt (MFW), caused by Fusarium oxysporum f. sp. melonis (Fom), is one of the most destructive diseases of melon (Cucumis melo L.). The development and deployment of resistant cultivars is generally considered to be the best approach to control MFW. Based on the host resistance genes associated with variants of this pathogen, Fom isolates were classified into four physiological races designated 0, 1, 2, and 1,2. Two dominant resistance genes, Fom-1 and Fom-2, control resistance to races 0 and 2, and 0 and 1, respectively. Fom isolates classified as race 1,2 are able to induce disease in melon lines carrying the above resistance genes. Many sources of resistance to Fom races 0, 1, and 2 have been reported. Partial resistance to race 1,2 controlled by polygenic recessive genes was only detected in a few Far Eastern melon accessions, except for the breeding line BIZ where complete resistance was described. Identification of DNA markers tightly linked to genes conferring resistance to Fom has immediate application in MFW resistance breeding programs. The Fom-2 gene has been cloned, and it encodes a protein with a nucleotide binding site (NBS) and leucine-rich repeats domain (LRR). Based on the sequence of this domain, some molecular markers linked to this gene were developed. Several DNA markers linked to Fom-1 have also been described. However, the usefulness of these markers was variety-dependent. Therefore, their combined use would be very useful in marker assisted selection for introducing resistance to Fom races 0 and 2 in melon. Recently, these markers were used for the positional cloning of this gene, which encoded a protein with a NBS–LRR domains that shows similarity to the toll and interleukin-1 receptores (TIR). Regarding Fom race 1,2, nine QTL were detected on five linkage groups by composite interval mapping. In this paper we review the current knowledge of MFW disease, and focus on genetic resistance to Fom and marker-assisted selection for resistance.

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Effect of Dinitroaniline Herbicides on Plant Resistance to Soilborne Pathogens

Cited by 28 publications

References 0 publications

Unexpected Side Effects of Herbicides: Modulation of Plant-Pathogen Interactions

Unexpected Side Effects of Herbicides: Modulation of Plant-Pathogen Interactions

Paclobutrazol and other plant growth‐retarding chemicals increase resistance of melon seedlings to fusarium wilt

Breeding melon for resistance to Fusarium wilt: recent developments

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