Inagaki Soichi, Nakamura Kenzo, Morikami Atsushi
Laboratory of Biochemistry, Graduate School of Bio-agricultural Sciences, Nagoya University, Chikusa, Nagoya, Japan.
PLoS Genet. 2009 Aug;5(8):e1000613. doi: 10.1371/journal.pgen.1000613. Epub 2009 Aug 21.
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.
发育过程中基因表达的时空调控取决于多种因素。拟南芥TEBICHI（TEB）基因发生突变，该基因编码含有假定解旋酶和DNA聚合酶结构域的蛋白质，会导致分生组织维持和正确器官形成出现缺陷，以及组成型DNA损伤反应和细胞周期进程缺陷；但teb突变体这些表型之间的分子联系尚不清楚。在这里，我们表明，DNA复制检查点途径基因ATR的突变，而不是ATM基因的突变，会增强teb突变体的发育表型，尽管atr抑制了teb突变体的细胞周期缺陷。参与同源重组的RAD51D和XRCC2基因的突变也会增强teb突变体的发育表型。teb和teb atr双突变体在叶片近轴-远轴极性上表现出缺陷，这部分是由ETTIN（ETT）/生长素响应因子3（ARF3）和ARF4基因的上调引起的。ETT/ARF3基因上游的Helitron转座子可能参与了teb中ETT/ARF3的上调。微阵列分析表明，teb和teb atr会导致Helitron转座子附近的基因优先上调。此外，有趣的是，重复基因，尤其是串联排列的同源基因，在teb或teb atr中高度上调。我们得出结论，TEB是DNA复制正常进行和发育过程中基因正确表达所必需的。将讨论这两种功能之间的相互作用以及导致特定基因表达改变的可能机制。
