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Gene duplication of type-B ARR transcription factors systematically extends transcriptional regulatory structures in Arabidopsis

ABSTRACT: Many of duplicated genes are enriched in signaling pathways. Recently, gene duplication of kinases has been shown to provide genetic buffering and functional diversification in cellular signaling. Transcription factors (TFs) are also often duplicated. However, how duplication of TFs affects their regulatory structures and functions of target genes has not been explored at the systems level. Here, we examined regulatory and functional roles of duplication of three major ARR TFs (ARR1, 10, and 12) in Arabidopsis cytokinin signaling using wild-type and single, double, and triple deletion mutants of the TFs. Comparative analysis of gene expression profiles obtained from Arabidopsis roots in wild-type and these mutants showed that duplication of ARR TFs systematically extended their transcriptional regulatory structures, leading to enhanced robustness and diversification in functions of target genes, as well as in regulation of cellular networks of target genes. Therefore, our results suggest that duplication of TFs contributes to robustness and diversification in functions of target genes by extending transcriptional regulatory structures.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE62597 | GEO | 2015/02/03

SECONDARY ACCESSION(S): PRJNA264518

REPOSITORIES: GEO

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Gene duplication of type-B ARR transcription factors systematically extends transcriptional regulatory structures in Arabidopsis

Project description:Many of duplicated genes are enriched in signaling pathways. Recently, gene duplication of kinases has been shown to provide genetic buffering and functional diversification in cellular signaling. Transcription factors (TFs) are also often duplicated. However, how duplication of TFs affects their regulatory structures and functions of target genes has not been explored at the systems level. Here, we examined regulatory and functional roles of duplication of three major ARR TFs (ARR1, 10, and 12) in Arabidopsis cytokinin signaling using wild-type and single, double, and triple deletion mutants of the TFs. Comparative analysis of gene expression profiles obtained from Arabidopsis roots in wild-type and these mutants showed that duplication of ARR TFs systematically extended their transcriptional regulatory structures, leading to enhanced robustness and diversification in functions of target genes, as well as in regulation of cellular networks of target genes. Therefore, our results suggest that duplication of TFs contributes to robustness and diversification in functions of target genes by extending transcriptional regulatory structures. Duplication of TFs can confer an extension of transcriptional regulatory structures for target genes by providing new regulatory relationships between duplicated TFs and new or old target genes. To examine the nature of the extension in the regulatory structure, we performed gene expression profiling of Arabidopsis root tissues obtained from wild-type (WT) and deletion mutants of three type-B ARR1, 10, and 12. To examine how the extended regulatory structures by the duplicated ARR TFs are utilized for the responses to external CK, we generated gene expression profiles of WT Arabidopsis roots treated with mock or exogenous CK for 1 hour. Total RNAs were isolated from two biological replicates at each condition and used to measure gene expression level.

2015-02-03 | E-GEOD-62597 | biostudies-arrayexpress

Arabidopsis thaliana

Project description:Gene duplication of type-B ARR transcription factors systematically extends transcriptional regulatory structures in Arabidopsis

| PRJNA264518 | ENA

The Ecoresponsive Genome of Daphnia pulex: Empirical annotation of the Daphnia pulex genome

Project description:This SuperSeries is composed of the following subset Series: GSE25841: Evolutionary Diversification of Duplicated Genes; Experiment A GSE25843: Evolutionary Diversification of Duplicated Genes; Experiments B-I, M-P GSE25845: Evolutionary Diversification of Duplicated Genes; Experiments B-I GSE25850: Evolutionary Diversification of Duplicated Genes; Experiment J GSE25851: Evolutionary Diversification of Duplicated Genes; Experiment L, K GSE25852: Empirical Annotation of the Daphnia pulex genome; Experiment B GSE25855: Empirical Annotation of the Daphnia pulex genome; Experiment A GSE25856: Empirical Annotation of the Daphnia pulex genome; Experiment C Refer to individual Series

2011-02-01 | E-GEOD-25823 | biostudies-arrayexpress

Interactome of Sec13 paralogs in Paradiplonema papillatum

Project description:The acquisition of new functions is frequently the result of gene duplication and is a major driver of evolutionary complexity. The β-propeller protein Sec13 plays roles in at least three distinct processes by virtue of being a component of the COPII endoplasmic reticulum export vesicle coat, the nuclear pore complex (NPC) and the Seh1-associated (SEA)/GATOR nutrient-sensing complex, suggesting that regulatory mechanisms coordinating these cellular activities may operate via Sec13. COPII, SEA and the NPC are ancient features of eukaryotic cells. We analyzed the Sec13 interactome in diplonemids, widespread marine protists, and found that Sec13 functions are divided between two paralogs, Sec13a and Sec13b. Sec13a interacts with COPII and the NPC, but by contrast Sec13b interacts with Sec16 and components of the SEA/GATOR complex. Hence, we infer that Sec13a is responsible for NPC functions and canonical anterograde transport activities while Sec13b acts within nutrient and autophagy-related pathways. Furthermore, duplication of Sec13 is near universal across the Euglenozoa, providing a potent exemplar of paralogy expansion and functional diversification.

2023-06-14 | PXD037122 | Pride

Daphnia pulex

Project description:Evolutionary Diversification of Duplicated Genes; Experiment A

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Project description:Evolutionary Diversification of Duplicated Genes; Experiment J

| PRJNA142491 | ENA

Daphnia pulex

Project description:Evolutionary Diversification of Duplicated Genes; Experiments B-I

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Daphnia pulex

Project description:Evolutionary Diversification of Duplicated Genes; Experiment L, K

| PRJNA142493 | ENA

Correction of the exon 2 duplication in DMD myoblasts by a single CRISPR/Cas9 system

Project description:Exonic duplications account for 10-15% of all mutations in Duchenne muscular dystrophy (DMD), a severe hereditary neuromuscular disorder. We report a novel CRISPR (Clustered Regularly Interspaced Short Palindromic Repeat)/Cas9-based strategy to correct the most frequent (exon 2) duplication in the DMD gene by targeted deletion, and tested the efficacy of such an approach in patient-derived myogenic cells. We demonstrate restoration of wild-type dystrophin expression at transcriptional and protein level in myotubes derived from genome-edited myoblasts in the absence of selection. Removal of the duplicated exon was achieved by the use of only one gRNA directed against an intronic duplicated region, thereby increasing editing efficiency and reducing the risk of off-target effects. This study opens a novel therapeutic perspective for patients carrying disease-causing duplications independently from the duplication extension.

2017-06-23 | GSE83658 | GEO

Fine mapping of a de novo interstitial 10q22-q23 duplication in a patient with congenital heart disease and microcephaly

Project description:In this study we report a female patient with an interstitial duplication of a region (10q22-q23) which is rarely reported in the literature. We fine mapped the duplication with array CGH, which revealed an 18.6 Mb duplication at 10q22.2-q23.33. There were no other deletions or duplication at another chromosome region. The duplicated region includes 89 annotated genes. The main clinical features of the patient are microcephaly and congenital heart disease. These are likely to be caused by dosage effect of one or several genes in the duplicated region. Finding of similar phenotypes in the other patients with 10q11-q22 duplications and in two out of three patients with 10q22-q23 duplications, suggest presence of genes involved in the development of these features at 10q22. Most of the duplication cases were investigated only by conventional chromosome analyses and fine mapping of these duplications will help identifying candidate genes/regions. Keywords: Array CGH

2007-10-01 | GSE8090 | GEO

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