Chlorsulfuron resistance in Daucus carota cell lines and plants:Involvement of gene amplification

Caretto, Sofia; Giardina, M. C.; Nicolodi, Chiara; Mariotti, D.

doi:10.1007/bf01240912

Cited by 36 publications

(22 citation statements)

References 23 publications

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“…With the exception of a few cases of gene amplification (Caretto et al, 1994), they originated in mutant germplasms obtained through tissue culture selection, seed or microspore mutagenesis, and even from wild relatives (Tan et al, 2005). Nothing is known about the side effects of these genes in crops.…”

Section: Introductionmentioning

confidence: 99%

Fitness costs linked to dinitroaniline resistance mutation in Setaria

Darmency¹,

Picard²,

Wang

2011

Heredity

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A mutant Thr-239-Ileu at the a2-tubulin gene was found to confer resistance to dinitroanilines, a family of mitosisdisrupting herbicides. However, mutations affecting microtubule polymerization and cell division are expected to impact growth and reproduction, that is, the fitness of a resistant weed or the yield of a tolerant crop, although it has not been demonstrated yet. This study was designed to test this hypothesis for the growth and reproduction of nearisogenic resistant and susceptible materials that were created in F 2 and F 3 generations after a Setaria viridis x S. italica cross. Differential growth was noticeable at the very onset of seedling growth. The homozygous resistant plants, grown both in a greenhouse cabinet and in the field, were smaller and had lower 1000-grain weight and therefore a lower yield. This fitness penalty is certainly due to modified cell division kinetics. Although the presence of the mutant allele accounted for 20% yield losses, there were also measurable benefits of dinitroaniline resistance, and these benefits are discussed.

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Section: Introductionmentioning

confidence: 99%

Fitness costs linked to dinitroaniline resistance mutation in Setaria

Darmency¹,

Picard²,

Wang

2011

Heredity

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“…37) Chlorsulfuron resistance in carrot cells is also associated with the increased activity of the target enzyme, acetohydroxyacid synthase, which is due to overproduction by gene ampliˆcation. 38) Thus, target enzyme overproduction in herbicide-resistant cells can lead to a higher en-zyme level which overcomes the toxic eŠects of the herbicide. Hence, the resistance to S23142 of YZI-1S cells could have been developed by overproduction of the target enzyme, mitochondrial Protox.…”

Section: Discussionmentioning

confidence: 99%

Resistance to Protoporphyrinogen Oxidase-inhibiting Compound S23142 from Overproduction of Mitochondrial Protoporphyrinogen Oxidase by Gene Amplification in Photomixotrophic Tobacco Cells

Watanabe

Takayama

Isogai

et al. 2002

Bioscience, Biotechnology, and Biochemistry

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Tobacco YZI-1S cells exhibit a 150-fold greater resistance to the protoporphyrinogen oxidase (Protox)-inhibiting compound, S23142, from wild-type tobacco cells. To investigate the mechanism for this S23142 resistance, the protein level, enzymatic activity, and sensitivity to S23142 in two Protox isoenzymes (plastidal and mitochondrial forms) were examined. The level of mitochondrial Protox protein was greater, and its activity 5-times higher, in YZI-IS cells than in wild-type cells. Furthermore, the apparent IC 50 value of S23142 was about 20 nM, which is 20-fold higher than that observed in wild-type cells. In contrast, no diŠerences were found in the plastidal Protox protein level, activity or its inhibition by S23142 between YZI-1S and wild-type cells. A southern blot analysis revealed that the mitochondrial Protox gene had been signiˆcantly ampliˆed in the YZI-1S cells. These results suggest that the S23142 resistance of YZI-1S cells was due to the overproduction of mitochondrial Protox by gene ampliˆcation.

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“…Na obtenção de culturas resistentes aos herbicidas, três estratégias podem ser utilizadas: transferência de genes que codificam enzima insensível ao herbicida, superprodução da enzima sensível e metabolização do herbicida (Merotto Jr. et al, 2000). No caso dos inibidores da ALS, utiliza-se, principalmente, o primeiro mecanismo, embora haja relatos da obtenção de mutantes em laboratório com aumento da expressão gênica em plantas de cenoura, através da superprodução da ALS (Caretto et al, 1994).…”

Section: Resistência De Culturas Aos Herbici-das Inibidores Da Alsunclassified

Resistência de plantas aos herbicidas inibidores da acetolactato sintase

et al. 2002

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A resistência de plantas aos herbicidas é conseqüência, na maioria das vezes, de mutação ou da preexistência de genes que conferem resistência à população. No caso dos herbicidas inibidores da acetolactato sintase (ALS) ocorreram casos de resistência tanto em plantas daninhas quanto em culturas. Essa revisão foi realizada com o objetivo de discutir aspectos bioquímicos, genéticos e moleculares da resistência de plantas aos herbicidas inibidores da ALS, sendo destacados também os efeitos na ecofisiologia das plantas daninhas e em mutações que conferem resistência em plantas daninhas e a possibilidade de utilizá-las para o desenvolvimento de culturas resistentes aos inibidores da ALS. Em plantas daninhas, a resistência aos herbicidas inibidores da ALS resulta de uma ou mais mutações no gene que codifica a ALS; quando a herança desse gene é monogênica, ele possui característica dominante a semidominante. As substituições em uma única seqüência nucleotídica ocasionam alteração na ALS, conferindo resistência aos herbicidas inibidores dessa enzima. Embora o biótipo resistente apresente alteração genética e enzimática quando comparado com biótipo suscetível, o comportamento ecofisiológico dos biótipos resistentes e suscetíveis é similar. Essa característica tem implicações muito importantes no estabelecimento das populações resistentes. Já foram desenvolvidos cultivares resistentes para diversas culturas, incluindo arroz e milho, as quais variam no nível de resistência aos diferentes grupos químicos de herbicidas inibidores da ALS.

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Chlorsulfuron resistance in Daucus carota cell lines and plants:Involvement of gene amplification

Cited by 36 publications

References 23 publications

Fitness costs linked to dinitroaniline resistance mutation in Setaria

Fitness costs linked to dinitroaniline resistance mutation in Setaria

Resistance to Protoporphyrinogen Oxidase-inhibiting Compound S23142 from Overproduction of Mitochondrial Protoporphyrinogen Oxidase by Gene Amplification in Photomixotrophic Tobacco Cells

Resistência de plantas aos herbicidas inibidores da acetolactato sintase

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