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.
Highlights
Many of duplicated genes are enriched in signaling pathways
Comparative analysis of gene expression profiles obtained from Arabidopsis roots in wild-type and these mutants showed that duplication of ARR Transcription factors (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
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
Summary
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. In C. albicans, the genes encoding LYS TFs (LYS14, 142, 143, and 144) are duplicated[11] Due to their sequence homology, they share common target genes, which can enhance robustness in regulation of their functions (genetic buffering). We analyzed how duplication of the three major type-B ARRs affects their transcriptional regulator structure and functions of their target genes at systems level. For this analysis, we used www.nature.com/scientificreports wild-type (WT) and single, double, and triple deletion mutants of ARR1, 10, and 12, as well as gene expression profiling of WT and these mutants
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