Relevant bibliographies by topics / Axr3-1 mutant

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Academic literature on the topic 'Axr3-1 mutant'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Axr3-1 mutant"

1

Cline, M. "NAA Restores Apical Dominance in the axr3-1 Mutant of Arabidopsis thaliana." Annals of Botany 87, no. 1 (January 2001): 61–65. http://dx.doi.org/10.1006/anbo.2000.1298.

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ROUX, FABRICE, and XAVIER REBOUD. "Is the cost of herbicide resistance expressed in the breakdown of the relationships between characters? A case study using synthetic-auxin-resistant Arabidopsis thaliana mutants." Genetical Research 85, no. 2 (April 2005): 101–10. http://dx.doi.org/10.1017/s0016672305007378.

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A mutation endowing herbicide resistance is often found to induce a parallel morphological or fitness penalty. To test whether such ‘cost’ of resistance to herbicides is expressed through lower resource acquisition, changes in resource allocation, or both, is of ecological significance. Here, we analysed 12 morphological traits in 900 plants covering three herbicide resistance mutations at genes AUX1, AXR1 and AXR2 in the model species Arabidopsis thaliana. Comparing these 2,4-D herbicide-resistant homozygous (RR) and heterozygous (RS) plants to homozygous susceptible (SS) plants, this analysis estimates the dominance level of the resistance allele on morphology. We also demonstrated that the herbicide resistance cost was primarily expressed as a change in resource acquisition (62·1–94% of the analysed traits). Although AUX1, AXR1 and AXR2 genes act in the same metabolic pathway of auxin response, each resistance factor was found to have its own unique signature in the way the cost was expressed. Furthermore, no link was observed between the absolute fitness penalty and the respective modifications of resource acquisition and/or resource allocation in the resistant plants. These results and their implications for herbicide resistance spread and establishment are discussed.
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Cernac, A., C. Lincoln, D. Lammer, and M. Estelle. "The SAR1 gene of Arabidopsis acts downstream of the AXR1 gene in auxin response." Development 124, no. 8 (April 15, 1997): 1583–91. http://dx.doi.org/10.1242/dev.124.8.1583.

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A screen for suppressors of the auxin resistant mutant axr1 in Arabidopsis thaliana has identified at least three second site suppressor loci called Suppressor of Auxin Resistance (SAR). In this study we focus on the SAR1 gene. Previous studies have documented the effects of the axr1 mutations on auxin-inhibition of root growth, auxin-induced gene expression, seedling morphology and aerial morphology. In this study, we show that the axr1 mutations also affect root hair development and epidermal cell length. The sar1-1 mutation suppresses at least partially, every aspect of the axr1 phenotype. Genetic experiments indicate that this suppression is gene specific. When crossed with the auxin-resistant mutant aux1-7, the suppressor has little affect on auxin response. However, the morphology of sar1-1 aux1-7 inflorescences is different from either of the single mutants indicating that both genes play a role in auxin mediated development of the inflorescence. The sar1-1 mutation also affects morphology in an AXR1 background. sar1-1 plants are shorter than wild-type, have altered leaf morphology, flower earlier than wild-type plants and appear to have reduced cell division in the primary root. In most respects sar1-1 axr1 and sar1 AXR1 plants are indistinguishable, indicating that sar1 both suppresses and is epistatic to axr1. Based on these results, we propose that SAR1 acts after AXR1 and that a major function of AXR1 is to relieve SAR1 mediated repression of auxin response.
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Timpte, C., A. K. Wilson, and M. Estelle. "The axr2-1 mutation of Arabidopsis thaliana is a gain-of-function mutation that disrupts an early step in auxin response." Genetics 138, no. 4 (December 1, 1994): 1239–49. http://dx.doi.org/10.1093/genetics/138.4.1239.

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Abstract The dominant axr2-1 mutation of Arabidopsis thaliana confers resistance to the plant hormones auxin, ethylene, and abscisic acid. In addition, axr2-1 has pleiotropic effects on plant morphology which include gravitropic defects in roots, hypocotyls and inflorescences of axr2-1 plants. Two genetic screens were conducted to isolate new mutations at the AXR2 locus. First, axr2-1 pollen was gamma-irradiated, crossed onto wild-type plants, and the M1 progeny screened for loss of the axr2-1 phenotype. Large deletions of the axr2-1 region on chromosome 3 resulted; however, none of these deletions appeared to be heritable. In the second, M2 seed obtained from axr2-1 gl-1 plants was screened for reversion of the axr2-1 phenotype. One revertant line, axr2-r3, has a distinctive phenotype caused by a second mutation at the axr2 locus. To learn more about the nature of the axr2-1 mutation, the effects of varying the ratio of wild-type to mutant copies of the AXR2 gene were examined by comparing plants of the following genotypes: +/+, +/+/+, axr2-1/axr2-1, axr2-1/+ and axr2-1/+/+. Additionally, accumulation of transcripts from the auxin-inducible SAUR-AC1 gene was examined to determine the response of wild-type and mutant plants to auxin. Wild-type seedlings and mature plants accumulate transcripts with auxin treatment. In contrast, axr2-1 tissue does not accumulate SAUR-AC1 transcripts in response to auxin. Taken together, these results indicate that axr2-1 is a neomorphic or hypermorphic mutation that disrupts an early step in an auxin response pathway.
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Wubben, Martin J. E., Hong Su, Steven R. Rodermel, and Thomas J. Baum. "Susceptibility to the Sugar Beet Cyst Nematode Is Modulated by Ethylene Signal Transduction in Arabidopsis thaliana." Molecular Plant-Microbe Interactions® 14, no. 10 (October 2001): 1206–12. http://dx.doi.org/10.1094/mpmi.2001.14.10.1206.

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Previously, we identified Arabidopsis thaliana mutant rhd1-4 as hypersusceptible to the sugar beet cyst nematode Heterodera schachtii. We assessed rhd1-4 as well as two other rhd1 alleles and found that each exhibited, in addition to H. schachtii hypersusceptibility, decreased root length, increased root hair length and density, and deformation of the root epidermal cells compared with wild-type A. thaliana ecotype Columbia (Col-0). Treatment of rhd1-4 and Col-0 with the ethylene inhibitors 2-aminoeth-oxyvinylglycine and silver nitrate and the ethylene precursor 1-aminocyclopropane-1-carboxylic acid suggests that the rhd1-4 hypersusceptibility and root morphology phenotypes are the result of an increased ethylene response. Assessment of known ethylene mutants further support the finding that ethylene plays a role in mediating A. thaliana susceptibility to H. schachtii because mutants that overproduce ethylene (eto1-1, eto2, and eto3) are hypersusceptible to H. schachtii and mutants that are ethylene-insensitive (etr1-1, ein2-1, ein3-1, eir1-1, and axr2) are less susceptible to H. schachtii. Because the ethylene mutants tested show altered susceptibility and altered root hair density and length, a discrimination between the effects of altered ethylene signal transduction and root hair density on susceptibility was accomplished by analyzing the ttg and gl2 mutants, which produce ectopic root hairs that result in greatly increased root hair densities while maintaining normal ethylene signal transduction. The observed normal susceptibilities to H. schachtii of ttg and gl2 indicate that increased root hair density, per se, does not cause hypersusceptibility. Furthermore, the results of nematode attraction assays suggest that the hypersusceptibility of rhd1-4 and the ethylene-overproducing mutant eto3 may be the result of increased attraction of H. schachtii-infective juveniles to root exudates of these plants. Our findings indicate that rhd1 is altered in its ethylene response and that ethylene signal transduction positively influences plant susceptibility to cyst nematodes.
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Barley, K. "Why hypocotyl extension mutants need to be characterized at the cell level: a case study of axr3-1." Journal of Experimental Botany 55, no. 399 (April 8, 2004): 1071–78. http://dx.doi.org/10.1093/jxb/erh115.

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López-Bucio, José, Juan Carlos Campos-Cuevas, Erasto Hernández-Calderón, Crisanto Velásquez-Becerra, Rodolfo Farías-Rodríguez, Lourdes Iveth Macías-Rodríguez, and Eduardo Valencia-Cantero. "Bacillus megaterium Rhizobacteria Promote Growth and Alter Root-System Architecture Through an Auxin- and Ethylene-Independent Signaling Mechanism in Arabidopsis thaliana." Molecular Plant-Microbe Interactions® 20, no. 2 (February 2007): 207–17. http://dx.doi.org/10.1094/mpmi-20-2-0207.

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Soil microorganisms are critical players in plant-soil interactions at the rhizosphere. We have identified a Bacillus megaterium strain that promoted growth and development of bean (Phaseolus vulgaris) and Arabidopsis thaliana plants. We used Arabidopsis thaliana as a model to characterize the effects of inoculation with B. megaterium on plant-growth promotion and postembryonic root development. B. megaterium inoculation caused an inhibition in primary-root growth followed by an increase in lateral-root number, lateral-root growth, and root-hair length. Detailed cellular analyses revealed that primary root-growth inhibition was caused both by a reduction in cell elongation and by reduction of cell proliferation in the root meristem. To study the contribution of auxin and ethylene signaling pathways in the alterations in root-system architecture elicited by B. megaterium, a suite of plant hormone mutants of Arabidopsis, including aux1-7, axr4-1, eir1, etr1, ein2, and rhd6, defective in either auxin or ethylene signaling, were evaluated for their responses to inoculation with this bacteria. When inoculated, all mutant lines tested showed increased biomass production. Moreover, aux1-7 and eir1, which sustain limited root-hair and lateral-root formation when grown in uninoculated medium, were found to increase the number of lateral roots and to develop long root hairs when inoculated with B. megaterium. The ethylene-signaling mutants etr1 and ein2 showed an induction in lateral-root formation and root-hair growth in response to bacterial inoculation. Taken together, our results suggest that plant-growth promotion and root-architectural alterations by B. megaterium may involve auxin- and-ethylene independent mechanisms.
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Vain, Thomas, Sara Raggi, Noel Ferro, Deepak Kumar Barange, Martin Kieffer, Qian Ma, Siamsa M. Doyle, et al. "Selective auxin agonists induce specific AUX/IAA protein degradation to modulate plant development." Proceedings of the National Academy of Sciences 116, no. 13 (March 8, 2019): 6463–72. http://dx.doi.org/10.1073/pnas.1809037116.

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Auxin phytohormones control most aspects of plant development through a complex and interconnected signaling network. In the presence of auxin, AUXIN/INDOLE-3-ACETIC ACID (AUX/IAA) transcriptional repressors are targeted for degradation by the SKP1-CULLIN1-F-BOX (SCF) ubiquitin-protein ligases containing TRANSPORT INHIBITOR RESISTANT 1/AUXIN SIGNALING F-BOX (TIR1/AFB). CULLIN1-neddylation is required for SCFTIR1/AFBfunctionality, as exemplified by mutants deficient in the NEDD8-activating enzyme subunit AUXIN-RESISTANT 1 (AXR1). Here, we report a chemical biology screen that identifies small molecules requiring AXR1 to modulate plant development. We selected four molecules of interest, RubNeddin 1 to 4 (RN1 to -4), among which RN3 and RN4 trigger selective auxin responses at transcriptional, biochemical, and morphological levels. This selective activity is explained by their ability to consistently promote the interaction between TIR1 and a specific subset of AUX/IAA proteins, stimulating the degradation of particular AUX/IAA combinations. Finally, we performed a genetic screen using RN4, the RN with the greatest potential for dissecting auxin perception, which revealed that the chromatin remodeling ATPase BRAHMA is implicated in auxin-mediated apical hook development. These results demonstrate the power of selective auxin agonists to dissect auxin perception for plant developmental functions, as well as offering opportunities to discover new molecular players involved in auxin responses.
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Romano, Charles P., Paul R. H. Robson, Harry Smith, Mark Estelle, and Harry Klee. "Transgene-mediated auxin overproduction in Arabidopsis: hypocotyl elongation phenotype and interactions with the hy6-1 hypocotyl elongation and axr1 auxin-resistant mutants." Plant Molecular Biology 27, no. 6 (March 1995): 1071–83. http://dx.doi.org/10.1007/bf00020881.

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10

Djami-Tchatchou, Arnaud T., Gregory A. Harrison, Chris P. Harper, Renhou Wang, Michael J. Prigge, Mark Estelle, and Barbara N. Kunkel. "Dual Role of Auxin in Regulating Plant Defense and Bacterial Virulence Gene Expression During Pseudomonas syringae PtoDC3000 Pathogenesis." Molecular Plant-Microbe Interactions® 33, no. 8 (August 2020): 1059–71. http://dx.doi.org/10.1094/mpmi-02-20-0047-r.

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Modification of host hormone biology is a common strategy used by plant pathogens to promote disease. For example, the bacterial pathogen strain Pseudomonas syringae DC3000 (PtoDC3000) produces the plant hormone auxin (indole-3-acetic acid [IAA]) to promote PtoDC3000 growth in plant tissue. Previous studies suggest that auxin may promote PtoDC3000 pathogenesis through multiple mechanisms, including both suppression of salicylic acid (SA)-mediated host defenses and via an unknown mechanism that appears to be independent of SA. To test if host auxin signaling is important during pathogenesis, we took advantage of Arabidopsis thaliana lines impaired in either auxin signaling or perception. We found that disruption of auxin signaling in plants expressing an inducible dominant axr2-1 mutation resulted in decreased bacterial growth and that this phenotype was suppressed by introducing the sid2-2 mutation, which impairs SA synthesis. Thus, host auxin signaling is required for normal susceptibility to PtoDC3000 and is involved in suppressing SA-mediated defenses. Unexpectedly, tir1 afb1 afb4 afb5 quadruple-mutant plants lacking four of the six known auxin coreceptors that exhibit decreased auxin perception, supported increased levels of bacterial growth. This mutant exhibited elevated IAA levels and reduced SA-mediated defenses, providing additional evidence that auxin promotes disease by suppressing host defense. We also investigated the hypothesis that IAA promotes PtoDC3000 virulence through a direct effect on the pathogen and found that IAA modulates expression of virulence genes, both in culture and in planta. Thus, in addition to suppressing host defenses, IAA acts as a microbial signaling molecule that regulates bacterial virulence gene expression.
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Dissertations / Theses on the topic "Axr3-1 mutant"

1

Kubalová, Monika. "Dynamika a role proteinu IAA17/AXR3 v regulaci růstu kořenů Arabidopsis thaliana auxinem." Master's thesis, 2020. http://www.nusl.cz/ntk/nusl-436400.

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Auxin is phytohormone that regulates several developmental processes and environmental responses. One of the most well-described outcome of the auxin signalling pathway is regulation of gene transcription. Aux/IAA proteins play an important role in this process, acting as transcriptional repressors. Recent studies revealed that several root growth responses are too rapid to be explained by changes in the level of transcription. The correlation between the amount of Aux/IAAs and the root growth rate suggests that these proteins might be involved in root growth regulation, especially during rapid growth responses that are not associated with transcriptional reprogramming. This work is focused on one of the 29 Arabidopsis Aux/IAA proteins - the IAA17/AXR3 protein. First, we produced stable transgenic lines of Arabidopsis thaliana expressing different combinations of fluorescently labelled AXR3-1 proteins and/or fused to subcellular localization tags under the control of different tissue-specific promoters, in order to characterize the subcellular localization of the studied protein. Subsequent visualization by confocal microscopy methods confirmed information about the role of IAA17/AXR3 protein in root growth responses, its involvement in auxin signalling, and gravitropism. Next, we showed that the...
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