ATM-mediated transcriptional and developmental responses to gamma-rays in Arabidopsis.
ATM-mediated transcriptional and developmental responses to gamma-rays in Arabidopsis.
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DOI：
10.1371/journal.pone.0000430
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发表时间：
2007-05-09
期刊：
影响因子：
3.7
通讯作者：
Montané MH
中科院分区：
文献类型：
--
作者：
Ricaud L;Proux C;Renou JP;Pichon O;Fochesato S;Ortet P;Montané MH
ATM（共济失调毛细血管扩张突变）是一种重要的检查点激酶，在真核生物中发出DNA双链断裂的信号。它的缺失导致拟南芥减数分裂和体细胞缺陷，并导致共济失调毛细血管扩张症（AT）患者的进行性运动障碍伴随着几种细胞缺陷。为了全面了解植物中的ATM途径，我们通过结合对野生型（WT）和纯合ATM缺陷突变体的根发育和全基因组表达谱的共聚焦激光扫描显微镜研究，对幼苗反应进行了时程分析。用剂量的γ射线（IR）对WT植物亚致死。在分生组织干细胞的早期形态缺陷表明，AtATM，拟南芥同源的人类ATM基因，是必不可少的，用于维持静止中心和控制初始细胞的分化后，暴露于IR。结果的几个微阵列实验进行了整个幼苗和根5小时后，IR编译在一个单一的表中，这是用来导入基因信息和提取基因集。序列和功能的同源性搜索;进口的时空，细胞周期，和mu-组成的表达特征;和一个简化的功能分类系统，用于确定新的基因在所有的功能类别。鉴定的数百个放射性调节基因不是随机收集的，而是属于功能途径，例如细胞周期;细胞死亡和修复; DNA复制，修复和重组;转录;翻译;和信号传导，表明ATM检查点的强大细胞重编程和双链断裂废除功能。因此，所有功能类别中的基因分别伴随着染色质脱乙酰酶的下调或乙酰化酶和甲基化酶的上调而下调或上调。确定与细胞增殖延迟或预期的后续生长素增加、加速细胞分化或死亡相一致的延长的S-G2期的早期转录指标，用于将IR调节的标志功能和IR后的组织表型联系起来。转录爆发几乎完全是AtATM依赖性的或弱AtATR依赖性的，并且遵循atm中表达的两个主要趋势：（i）-损失或严重衰减和延迟，以及（ii）-反向和/或随机以及特定，使人们能够区分IR/ATM路径成分。我们的数据提供了一个大的资源，植物细胞周期，发育，激素反应和DNA修复功能的检查点之间的相互作用的研究，因为IR诱导的转录变化部分重叠与环境胁迫的反应。ATM与IR后干细胞维持途径的假定联系也进行了讨论。
ATM (Ataxia Telangiectasia Mutated) is an essential checkpoint kinase that signals DNA double-strand breaks in eukaryotes. Its depletion causes meiotic and somatic defects in Arabidopsis and progressive motor impairment accompanied by several cell deficiencies in patients with ataxia telangiectasia (AT). To obtain a comprehensive view of the ATM pathway in plants, we performed a time-course analysis of seedling responses by combining confocal laser scanning microscopy studies of root development and genome-wide expression profiling of wild-type (WT) and homozygous ATM-deficient mutants challenged with a dose of γ-rays (IR) that is sublethal for WT plants. Early morphologic defects in meristematic stem cells indicated that AtATM, an Arabidopsis homolog of the human ATM gene, is essential for maintaining the quiescent center and controlling the differentiation of initial cells after exposure to IR. Results of several microarray experiments performed with whole seedlings and roots up to 5 h post-IR were compiled in a single table, which was used to import gene information and extract gene sets. Sequence and function homology searches; import of spatio-temporal, cell cycling, and mutant-constitutive expression characteristics; and a simplified functional classification system were used to identify novel genes in all functional classes. The hundreds of radiomodulated genes identified were not a random collection, but belonged to functional pathways such as those of the cell cycle; cell death and repair; DNA replication, repair, and recombination; and transcription; translation; and signaling, indicating the strong cell reprogramming and double-strand break abrogation functions of ATM checkpoints. Accordingly, genes in all functional classes were either down or up-regulated concomitantly with downregulation of chromatin deacetylases or upregulation of acetylases and methylases, respectively. Determining the early transcriptional indicators of prolonged S-G2 phases that coincided with cell proliferation delay, or an anticipated subsequent auxin increase, accelerated cell differentiation or death, was used to link IR-regulated hallmark functions and tissue phenotypes after IR. The transcription burst was almost exclusively AtATM-dependent or weakly AtATR-dependent, and followed two major trends of expression in atm: (i)-loss or severe attenuation and delay, and (ii)-inverse and/or stochastic, as well as specific, enabling one to distinguish IR/ATM pathway constituents. Our data provide a large resource for studies on the interaction between plant checkpoints of the cell cycle, development, hormone response, and DNA repair functions, because IR-induced transcriptional changes partially overlap with the response to environmental stress. Putative connections of ATM to stem cell maintenance pathways after IR are also discussed.
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影响因子：
11.4
作者：
Aylon, Y;Liefshitz, B;Kupiec, M
通讯作者：
Kupiec, M
影响因子：
64.8
作者：
Blilou, I;Xu, J;Scheres, B
通讯作者：
Scheres, B
DOI：
10.1083/jcb.200510130
发表时间：
2006-04-24
期刊：
The Journal of cell biology
影响因子：
--
作者：
Bekker-Jensen S;Lukas C;Kitagawa R;Melander F;Kastan MB;Bartek J;Lukas J
通讯作者：
Lukas J
影响因子：
7.2
作者：
Colón-Carmona, A;You, R;Doerner, P
通讯作者：
Doerner, P
DOI：
10.1111/j.2517-6161.1995.tb02031.x
发表时间：
1995-01-01
影响因子：
5.8
作者：
BENJAMINI, Y;HOCHBERG, Y
通讯作者：
HOCHBERG, Y