auxin/imunopatologické reakce

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Ectopic expression of miR160 results in auxin hypersensitivity, cytokinin hyposensitivity, and inhibition of symbiotic nodule development in soybean.

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Symbiotic root nodules in leguminous plants result from interaction between the plant and nitrogen-fixing rhizobia bacteria. There are two major types of legume nodules, determinate and indeterminate. Determinate nodules do not have a persistent meristem, while indeterminate nodules have a

Mutations in the TIR1 auxin receptor that increase affinity for auxin/indole-3-acetic acid proteins result in auxin hypersensitivity.

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The phytohormone auxin regulates virtually every aspect of plant development. The hormone directly mediates the interaction between the two members of the auxin coreceptor complex, a TRANSPORT INHIBITOR RESPONSE (TIR1)/AUXIN SIGNALING F-BOX protein and an AUXIN/INDOLE-3-ACETIC ACID (Aux/IAA)

Auxin and light control of adventitious rooting in Arabidopsis require ARGONAUTE1.

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Adventitious rooting is a quantitative genetic trait regulated by both environmental and endogenous factors. To better understand the physiological and molecular basis of adventitious rooting, we took advantage of two classes of Arabidopsis thaliana mutants altered in adventitious root formation:

Arabidopsis cytokinin-resistant mutant, cnr1, displays altered auxin responses and sugar sensitivity.

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Based upon the phenotype of young, dark-grown seedlings, a cytokinin-resistant mutant, cnr1, has been isolated, which displays altered cytokinin- and auxin-induced responses. The mutant seedlings possess short hypocotyls and open apical hooks (in dark), and display agravitropism, hyponastic

Overexpression of RAN1 in rice and Arabidopsis alters primordial meristem, mitotic progress, and sensitivity to auxin.

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Ran is an evolutionarily conserved eukaryotic GTPase. We previously identified a cDNA of TaRAN1, a novel Ran GTPase homologous gene in wheat (Triticum aestivum) and demonstrated that TaRAN1 is associated with regulation of genome integrity and cell division in yeast (Saccharomyces cerevisiae)

The 5'-3' Exoribonuclease XRN4 Regulates Auxin Response via the Degradation of Auxin Receptor Transcripts.

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Auxin is a major hormone which plays crucial roles in instructing virtually all developmental programs of plants. Its signaling depends primarily on its perception by four partially redundant receptors of the TIR1/AFB2 clade (TAARs), which subsequently mediate the specific degradation of AUX/IAA

Expression Profiling of Strawberry Allergen Fra a during Fruit Ripening Controlled by Exogenous Auxin.

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Strawberry fruit contain the allergenic Fra a proteins, members of the pathogenesis-related 10 protein family that causes oral allergic syndrome symptoms. Fra a proteins are involved in the flavonoid biosynthesis pathway, which might be important for color development in fruits. Auxin is an

The AFB4 auxin receptor is a negative regulator of auxin signaling in seedlings.

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The plant hormone auxin is perceived by a family of F box proteins called the TIR1/auxin-signaling F box proteins (AFBs). Phylogenetic studies reveal that these proteins fall into four clades in flowering plants called TIR1, AFB2, AFB4, and AFB6. Genetic studies indicate that members of the TIR1 and

Reduced expression of AtNUP62 nucleoporin gene affects auxin response in Arabidopsis.

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BACKGROUND The plant nuclear pore complex has strongly attracted the attention of the scientific community during the past few years, in particular because of its involvement in hormonal and pathogen/symbiotic signalling. In Arabidopsis thaliana, more than 30 nucleoporins have been identified, but

Mutants of Nicotiana plumbaginifolia with increased sensitivity to auxin.

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Two non-allelic, monogenic recessive mutations, aus1 and aus2, have been isolated which result in auxin hypersensitivity in mutant Nicotiana plumbaginifolia plants. At relatively low concentrations of indole-3-acetic acid or 1-naphthaleneacetic acid, the elongation growth of mutant seedling

PIS1, a negative regulator of the action of auxin transport inhibitors in Arabidopsis thaliana.

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In order to clarify the mechanism underlying the polar auxin transport system, the pis1 mutant in Arabidopsis thaliana that is hypersensitive to N-1-naphthylphthalamic acid (NPA), an auxin transport inhibitor was isolated and characterized. Whereas the pis1 mutant is normally sensitive to

ATAF2, a NAC transcription factor, binds to the promoter and regulates NIT2 gene expression involved in auxin biosynthesis.

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The transcription factor ATAF2, one of the plant specific NAC family genes, is known as repressor of pathogenesis-related genes and responsive to the diverse defense-related hormones, pathogen infection, and wounding stress. Furthermore, it is important to consider that tryptophan-dependant IAA

Overexpression of plum auxin receptor PslTIR1 in tomato alters plant growth, fruit development and fruit shelf-life characteristics.

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BACKGROUND TIR1-like proteins are F-box auxin receptors. Auxin binding to the F-box receptor proteins promotes the formation of SCF(TIR1) ubiquitin ligase complex that targets the auxin repressors, Aux/IAAs, for degradation via the ubiquitin/26S proteasome pathway. The release of auxin response

The beta-subunit of the Arabidopsis G protein negatively regulates auxin-induced cell division and affects multiple developmental processes.

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Plant cells respond to low concentrations of auxin by cell expansion, and at a slightly higher concentration, these cells divide. Previous work revealed that null mutants of the alpha-subunit of a putative heterotrimeric G protein (GPA1) have reduced cell division. Here, we show that this

Two homologous ATP-binding cassette transporter proteins, AtMDR1 and AtPGP1, regulate Arabidopsis photomorphogenesis and root development by mediating polar auxin transport.

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Light and auxin control many aspects of plant growth and development in an overlapping manner. We report here functional characterization of two closely related ABC (ATP-binding cassette) transporter genes, AtMDR1 and AtPGP1, in light and auxin responses. We showed that loss-of-function atmdr1 and

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