A link among DNA replication, recombination, and gene expression revealed by genetic and genomic analysis of TEBICHI gene of Arabidopsis thaliana.

A link among DNA replication, recombination, and gene expression revealed by genetic and genomic analysis of TEBICHI gene of Arabidopsis thaliana.
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DOI:
10.1371/journal.pgen.1000613
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发表时间:
2009-08
期刊:
影响因子:
4.5
通讯作者:
Morikami A
Morikami A
中科院分区:
生物学2区
文献类型:
--
作者:
Inagaki S;Nakamura K;Morikami A

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发育过程中基因表达的时空调控取决于许多因素。拟南芥TEBICHI(TEB)基因编码的解旋酶和DNA聚合酶结构域蛋白的突变导致分生组织维持和正确器官形成的缺陷,以及组成性DNA损伤反应和细胞周期进程的缺陷;但这些teb突变体表型之间的分子联系尚不清楚。在这里,我们表明,突变的DNA复制检查点途径基因,ATR,而不是在ATM基因,增强发育表型的teb突变体,虽然ATR抑制细胞周期缺陷的teb突变体。teb突变体的发育表型也通过参与同源重组的RAD 51 D和XRCC 2基因的突变而增强。teb和teb atr双突变体表现出叶片近轴-远轴极性的缺陷,这部分是由ETTIN(ETT)/生长素反应因子3(ARF 3)和ARF 4基因的上调引起的。ETT/ARF 3基因上游的Helitron转座子可能参与了TEB中ETT/ARF 3基因的上调。微阵列分析表明,teb和teb atr导致Helitron转座子附近的基因的优先上调。此外,有趣的是,重复基因,特别是串联排列的同源基因,在teb或teb atr中高度上调。我们的结论是,TEB是所需的DNA复制的正常进展,并在发展过程中的基因的正确表达。这两个功能之间的相互作用和可能的机制,导致特定基因的表达改变将进行讨论。DNA复制、修复和重组是相互关联的过程。染色质结构,其中DNA包装,是重要的DNA复制,修复和重组的调节,以及基因转录。DNA复制和修复后,染色质状态(包括其结构和修饰)必须重现,这些过程中的缺陷可能会由于染色质调节的变化而改变基因表达程序。我们对模式植物拟南芥tebichi(teb)突变体的一系列遗传分析表明,TEB基因参与DNA的复制和重组。我们还发现TEB基因是许多基因包括发育调控基因正确表达所必需的。从这些结果中,我们提出,TEB基因的功能是重要的DNA复制和重组后的基因表达模式的维护。此外,在teb突变体中观察到高度重复的转座子和串联排列的同源基因附近的基因优先上调,这表明重复序列周围的同源重组和基因转录之间的相互关系。
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, are highly upregulated in teb or teb atr. We conclude that TEB is required for normal progression of DNA replication and for correct expression of genes during development. Interplay between these two functions and possible mechanism leading to altered expression of specific genes will be discussed. DNA replication, repair, and recombination are interrelated processes. Chromatin structure, into which DNA is packaged, is important for regulation of DNA replication, repair, and recombination, as well as gene transcription. After DNA replication and repair, chromatin status including its structure and modification has to be reproduced, and defects in these processes can alter gene expression program because of change in chromatin regulation. Our series of genetic analysis of tebichi (teb) mutant of model plant Arabidopsis thaliana suggest that TEB gene is involved in DNA replication and recombination. We also show here that TEB gene is required for correct expression of many genes including genes regulating development. From these results we propose that TEB gene function is important for maintenance of gene expression pattern after DNA replication and recombination. Furthermore, preferential upregulation of genes near highly duplicated transposons and tandemly arrayed homologous genes are observed in teb mutants, suggesting the interrelationship between homologous recombination and gene transcription around the repetitive sequences.
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发表时间: 1999-11-01
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