Abstract:ERFs (ethylene-responsive element binding factors) belong to a large family of plant transcription factors that are found exclusively in plants. A small subfamily of ERF proteins can act as transcriptional repressors. The Arabidopsis genome contains eight ERF repressors, namely AtERF3, AtERF4, and AtERF7 to AtERF12. Members of ERF repressors show differential expression, suggesting that they may have different function. Using a transient expression system, we demonstrated that AtERF4, AtERF7, AtERF10, AtERF11 … Show more
“…Constitutive receptor signaling in Arabidopsis ethylene receptor gain-of-function mutants etr1-1 and ein4-1 also promotes expression of these genes. Recently, AtERF4 has been found to be a transcriptional repressor conferring ethylene insensitivity in its transgenic Arabidopsis plants, and the AtERF4-overexpressing plants are hypersensitive to sodium chloride (McGrath et al, 2005;Yang et al, 2005). This observation is consistent with our present findings.…”
Ethylene signaling plays important roles in multiple aspects of plant growth and development. Its functions in abiotic stress responses remain largely unknown. Here, we report that alteration of ethylene signaling affected plant salt-stress responses. A type II ethylene receptor homolog gene NTHK1 (Nicotiana tabacum histidine kinase 1) from tobacco (N. tabacum) conferred salt sensitivity in NTHK1-transgenic Arabidopsis (Arabidopsis thaliana) plants as judged from the phenotypic change, the relative electrolyte leakage, and the relative root growth under salt stress. Ethylene precursor 1-aminocyclopropane-1-carboxylic acid suppressed the salt-sensitive phenotype. Analysis of Arabidopsis ethylene receptor gain-of-function mutants further suggests that receptor function may lead to salt-sensitive responses. Mutation of EIN2, a central component in ethylene signaling, also results in salt sensitivity, suggesting that EIN2-mediated signaling is beneficial for plant salt tolerance. Overexpression of the NTHK1 gene or the receptor gain-of-function activated expression of salt-responsive genes AtERF4 and Cor6.6. In addition, the transgene NTHK1 mRNA was accumulated under salt stress, suggesting a posttranscriptional regulatory mechanism. These findings imply that ethylene signaling may be required for plant salt tolerance.
“…Constitutive receptor signaling in Arabidopsis ethylene receptor gain-of-function mutants etr1-1 and ein4-1 also promotes expression of these genes. Recently, AtERF4 has been found to be a transcriptional repressor conferring ethylene insensitivity in its transgenic Arabidopsis plants, and the AtERF4-overexpressing plants are hypersensitive to sodium chloride (McGrath et al, 2005;Yang et al, 2005). This observation is consistent with our present findings.…”
Ethylene signaling plays important roles in multiple aspects of plant growth and development. Its functions in abiotic stress responses remain largely unknown. Here, we report that alteration of ethylene signaling affected plant salt-stress responses. A type II ethylene receptor homolog gene NTHK1 (Nicotiana tabacum histidine kinase 1) from tobacco (N. tabacum) conferred salt sensitivity in NTHK1-transgenic Arabidopsis (Arabidopsis thaliana) plants as judged from the phenotypic change, the relative electrolyte leakage, and the relative root growth under salt stress. Ethylene precursor 1-aminocyclopropane-1-carboxylic acid suppressed the salt-sensitive phenotype. Analysis of Arabidopsis ethylene receptor gain-of-function mutants further suggests that receptor function may lead to salt-sensitive responses. Mutation of EIN2, a central component in ethylene signaling, also results in salt sensitivity, suggesting that EIN2-mediated signaling is beneficial for plant salt tolerance. Overexpression of the NTHK1 gene or the receptor gain-of-function activated expression of salt-responsive genes AtERF4 and Cor6.6. In addition, the transgene NTHK1 mRNA was accumulated under salt stress, suggesting a posttranscriptional regulatory mechanism. These findings imply that ethylene signaling may be required for plant salt tolerance.
“…The remaining gene, VTC5, has no known defense role, but its coexpression with these other defense regulators makes this a viable hypothesis. Interestingly, ERF4 mediates antagonism between the ET and ABA pathways with overexpression of ERF4 leading to decreased sensitivity to ABA (Yang et al, 2005).…”
Transcriptional reprogramming forms a major part of a plant's response to pathogen infection. Many individual components and pathways operating during plant defense have been identified, but our knowledge of how these different components interact is still rudimentary. We generated a high-resolution time series of gene expression profiles from a single Arabidopsis thaliana leaf during infection by the necrotrophic fungal pathogen Botrytis cinerea. Approximately one-third of the Arabidopsis genome is differentially expressed during the first 48 h after infection, with the majority of changes in gene expression occurring before significant lesion development. We used computational tools to obtain a detailed chronology of the defense response against B. cinerea, highlighting the times at which signaling and metabolic processes change, and identify transcription factor families operating at different times after infection. Motif enrichment and network inference predicted regulatory interactions, and testing of one such prediction identified a role for TGA3 in defense against necrotrophic pathogens. These data provide an unprecedented level of detail about transcriptional changes during a defense response and are suited to systems biology analyses to generate predictive models of the gene regulatory networks mediating the Arabidopsis response to B. cinerea.
“…However, these genes showed differential expression and distinct roles in plant growth and development as well as in response to environmental stress. For instance, the ERF4 and ERF7 genes play an important role in the response to ABA (Yang et al, 2005;Song et al, 2005). The overexpression of ERF7 increased the sensitivity to ABA in guard cells (Song et al, 2005).…”
Section: Tabel 1 Marka Ekspresi Gen (Gems) Dari Ap2/erf Saat Penyadamentioning
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