a link among dna replication, recombination, and gene expression revealed by genetic and genomic analysis of tebichi gene of arabidopsis thaliana链接在dna复制、重组和基因表达基因和基因组的分析揭示了tebichi拟南芥的基因.pdfVIP

a link among dna replication, recombination, and gene expression revealed by genetic and genomic analysis of tebichi gene of arabidopsis thaliana链接在dna复制、重组和基因表达基因和基因组的分析揭示了tebichi拟南芥的基因.pdf

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a link among dna replication, recombination, and gene expression revealed by genetic and genomic analysis of tebichi gene of arabidopsis thaliana链接在dna复制、重组和基因表达基因和基因组的分析揭示了tebichi拟南芥的基因

A Link among DNA Replication, Recombination, and Gene Expression Revealed by Genetic and Genomic Analysis of TEBICHI Gene of Arabidopsis thaliana 1¤ 1 2 Soichi Inagaki *, Kenzo Nakamura , Atsushi Morikami 1 Laboratory of Biochemistry, Graduate School of Bio-agricultural Sciences, Nagoya University, Chikusa, Nagoya, Japan, 2 Faculty of Agriculture, Meijo University, Tenpaku, Nagoya, Japan Abstract Spatio-temporal regulation of gene expression during development depends on many factors. Mutations in Arabidopsis thaliana TEBICHI (TEB) gene encoding putative helicase and DNA polymerase domains-containing protein result in defects in meristem maintenance and correct organ formation, as well as constitutive DNA damage response and a defect in cell cycle progression; but the molecular link between these phenotypes of teb mutants is unknown. Here, we show that mutations in the DNA replication checkpoint pathway gene, ATR, but not in ATM gene, enhance developmental phenotypes of teb mutants, although atr suppresses cell cycle defect of teb mutants. Developmental phenotypes of teb mutants are also enhanced by mutations in RAD51D and XRCC2 gene, which are involved in homologous recombination. teb and teb atr double mutants exhibit defects in adaxial-abaxial polarity of leaves, which is caused in part by the upregulation of ETTIN (ETT)/AUXIN RESPONSIVE FACTOR 3 (ARF3) and ARF4 genes. The Helitron transposon in the upstream of ETT/ARF3 gene is likely to be involved in the upregulation of ETT/ARF3 in teb. Microarray analysis indicated that teb and teb atr causes preferential upregulation of genes nearby the Helitron transposons. Furthermore, interestingly, duplicated genes, especially tandemly arrayed homologous genes

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