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Genetics and epigenetics in flower pigmentation associated with transposable elements in morning glories. 牵牛花色素沉着与转座因子相关的遗传学和表观遗传学。
Pub Date : 2004-01-01
Shigeru Iida, Yasumasa Morita, Jeong-Doo Choi, Kyeung-Il Park, Atsushi Hoshino

Among the genus Ipomoea, three morning glories, I. nil (the Japanese morning glory), I. purpurea (the common morning glory), and I. tricolor, were domesticated well for floricultural plants, and many spontaneous mutants displaying various flower pigmentation patterns were isolated. Most of these spontaneous mutations were found to be caused by the insertion of DNA transposable elements in the genes for the anthocyanin pigmentation in flowers, and many of them exhibited variegated flowers, such as white flowers with pigmented spots and sectors. Here, we describe the historical background of the mutants displaying variegated flowers and review the genetic and epigenetic regulation in flower pigmentation associated with transposable elements of these morning glories. The flecked, speckled, r-1, and purple mutations in I. nil were caused by insertions of Tpn1 and its relatives in the En/Spm superfamily, Tpn2, Tpn3, and Tpn4, into the genes for anthocyanin coloration in flowers, i.e., DFR-B, CHI, CHS-D, and InNHX1, respectively. Similarly, the flaked and pink mutants of I. purpurea have distantly related elements, Tip100 and Tip201, in the Ac/Ds superfamily inserted into the CHS-D and F3'H genes, respectively. The flower variegation patterns can be determined by the frequency and timing of the excision of these transposons, and their stable insertions produce plain color flowers without generating pigmented spots or sectors; furthermore, both genetic and epigenetic regulation appeared to play important roles in determining the frequency and timing of the excision of the transposons. However, flower variegation is not always associated with the excision of an integrated DNA transposon from one of the genes for anthocyanin pigmentation. The mutant Flying Saucers of I. tricolor displaying variegated flowers was found to have the transposon ItMULE1 inserted into the DFR-B promoter region, but no excision of ItMULE1 from the DFR-B could be detected in the variegated flower lines. The instable pearly-vrg allele in cv. Flying Saucers is likely to be an epiallele because the DNA methylation in the DFR-B promoter appeared to be associated with flower pigmentation.

在易普莫亚属植物中,三种牵牛花,日本牵牛花,紫花牵牛花和三色牵牛花被驯化得很好,并分离出许多具有不同花色素模式的自发突变体。这些自发突变大多是由于在花中花青素色素沉着基因中插入DNA转座元件引起的,其中许多突变呈现出杂色花,如带有色素斑点和扇形的白色花。在这里,我们描述了显示杂色花的突变体的历史背景,并回顾了与这些牵牛花转座因子相关的花色素的遗传和表观遗传调控。I. nil的斑点突变、斑点突变、r-1突变和紫色突变是由Tpn1及其En/Spm超家族的近缘基因Tpn2、Tpn3和Tpn4分别插入花中花青素着色基因DFR-B、CHI、CHS-D和InNHX1引起的。同样,紫花紫豆的片状突变体和粉红色突变体在Ac/Ds超家族中分别有插入CHS-D和F3'H基因的远亲元件Tip100和Tip201。这些转座子的切除频率和时间决定了花的斑驳模式,它们稳定的插入产生素色花,不产生色素斑点或扇形;此外,遗传和表观遗传调控似乎在确定转座子切除的频率和时间方面发挥重要作用。然而,花的杂色并不总是与从花青素色素沉着基因之一的整合DNA转座子的切除有关。三色鸢尾花突变体Flying Saucers在DFR-B启动子区插入了转座子ItMULE1,但在杂色花系中未检测到ItMULE1从DFR-B中移除。不稳定的珍珠vrg等位基因。飞碟很可能是一个外等位基因,因为DFR-B启动子中的DNA甲基化似乎与花色素沉着有关。
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引用次数: 0
Gpt delta transgenic mouse: A novel approach for molecular dissection of deletion mutations in vivo Gpt δ转基因小鼠:体内缺失突变分子解剖的新方法
Pub Date : 2004-01-01 DOI: 10.1016/S0065-227X(04)80106-0
Takehiko Nohmi, Ken-Ichi Masumura

Human genome is continuously exposed to various DNA damaging agents including reactive oxygen species. Of various forms of DNA damage, double-strand breaks (DSBs) in DNA are the most detrimental because of the mutagenicity and cytotoxicity. To combat the serious threats posed by DSBs, cells evolved various homologous and non-homologous recombination repair mechanisms. However, some repair mechanisms appear to be involved in the induction of genome rearrangements such as deletions. To analyze the deletion mutations in a whole body system, gpt delta mice were established. In this mouse model, deletions in λ, DNA integrated in the chromosome are preferentially selected as Spi phages, which can then be subjected for molecular analysis. Here, we reported the sequence characteristics of deletions induced by ionizing radiations in the liver, ultraviolet light β in the epidermis, mitomycin C in the bone marrow and heterocyclic amine PhIP in the colon. To our knowledge, this is the first report in which in vivo deletion mutations are systematically analyzed at the molecular level. About half of the large deletions occur between short direct-repeat sequences and the remainder had flush ends, suggesting that they are generated during the repair of DSBs in DNA. The results also suggest that mutation induction and repair mechanisms may vary depending on the type of organs/tissues examined, i.e., germ cells versus somatic cells or highly proliferating cells versus slowly proliferating cells. Possible mechanisms of intrachromosomal deletion mutations are discussed.

人类基因组持续暴露于包括活性氧在内的各种DNA损伤剂中。在各种形式的DNA损伤中,DNA的双链断裂(DSBs)是最有害的,因为它具有诱变性和细胞毒性。为了对抗DSBs的严重威胁,细胞进化出各种同源和非同源重组修复机制。然而,一些修复机制似乎涉及到基因组重排的诱导,如缺失。为了分析整个系统的缺失突变,我们建立了gpt delta小鼠。在该小鼠模型中,整合在染色体上的DNA λ缺失被优先选择为Spi -噬菌体,然后可以进行分子分析。在这里,我们报道了肝脏电离辐射、表皮紫外光β、骨髓丝裂霉素C和结肠杂环胺PhIP诱导的缺失的序列特征。据我们所知,这是第一个在分子水平上系统分析体内缺失突变的报告。大约一半的大缺失发生在短的直接重复序列之间,其余的有同源末端,这表明它们是在DNA中dsb的修复过程中产生的。结果还表明,突变诱导和修复机制可能因所检查的器官/组织类型而异,即生殖细胞与体细胞或高增殖细胞与慢增殖细胞。讨论了染色体内缺失突变的可能机制。
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引用次数: 32
Cell death promoted by homologous DNA interaction from bacteria to humans 从细菌到人的同源DNA相互作用促进细胞死亡
Pub Date : 2004-01-01 DOI: 10.1016/S0065-227X(04)80091-1
Kohji Kusano

Pairing between homologous DNA controls cellular functions including double-strand break repair, mitotic recombination, and progression of DNA replication forks, as well as chiasma formation during meiosis. Here I summarize that homologous interaction could promote the cell killing in bacteria, yeast, and multicellular organisms. The mechanisms of cell killing are categorized into two types: (1) the killing due to the accumulation of extrachromosomal DNA; (2) the killing induced by Holliday junction structures. I propose that the mechanisms of such killing function as novel apoptotic pathways in the cells carrying severe DNA damages to eliminate such damages from cell population.

同源DNA之间的配对控制着细胞功能,包括双链断裂修复、有丝分裂重组和DNA复制叉的进展,以及减数分裂期间交叉的形成。本文总结了同源相互作用在细菌、酵母和多细胞生物中促进细胞杀伤的研究进展。细胞杀伤机制可分为两种类型:(1)染色体外DNA的累积杀伤;(2) Holliday结结构引起的杀伤。我提出这种杀伤功能的机制是在携带严重DNA损伤的细胞中出现新的凋亡途径,以消除细胞群中的这种损伤。
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引用次数: 0
Cell death promoted by homologous DNA interaction from bacteria to humans. 从细菌到人的同源DNA相互作用促进细胞死亡。
Pub Date : 2004-01-01
Kohji Kusano

Pairing between homologous DNA controls cellular functions including double-strand break repair, mitotic recombination, and progression of DNA replication forks, as well as chiasma formation during meiosis. Here I summarize that homologous interaction could promote the cell killing in bacteria, yeast, and multicellular organisms. The mechanisms of cell killing are categorized into two types: (1) the killing due to the accumulation of extrachromosomal DNA; (2) the killing induced by Holliday junction structures. I propose that the mechanisms of such killing function as novel apoptotic pathways in the cells carrying severe DNA damages to eliminate such damages from cell population.

同源DNA之间的配对控制着细胞功能,包括双链断裂修复、有丝分裂重组和DNA复制叉的进展,以及减数分裂期间交叉的形成。本文总结了同源相互作用在细菌、酵母和多细胞生物中促进细胞杀伤的研究进展。细胞杀伤机制可分为两种类型:(1)染色体外DNA的累积杀伤;(2) Holliday结结构引起的杀伤。我提出这种杀伤功能的机制是在携带严重DNA损伤的细胞中出现新的凋亡途径,以消除细胞群中的这种损伤。
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引用次数: 0
Illegitimate recombination mediated by double-strand break and end-joining in Escherichia coli. 大肠杆菌双链断裂和末端连接介导的不正当重组。
Pub Date : 2004-01-01
Hideo Ikeda, Kouya Shiraishi, Yasuyuki Ogata

The frequency of illegitimate recombination has been measured by a lambdabio transducing phage assay during the induction of the E. coli lambda c1857 lysogen. Illegitimate recombination falls into two classes, short homology-independent and short homology-dependent illegitimate recombination. The former involves sequences with virtually no homology, and is mediated by DNA topoisomerases and controlled by the DNA binding protein HU. The latter is induced by UV irradiation or other DNA damaging agents and requires short regions of homology, usually contain 4 to 13 base pairs, at sites involved in recombination. It has been shown that the RecJ exonuclease promotes short homology-dependent illegitimate recombination, but that the RecQ helicase suppresses it. In addition, we have shown that the overexpression of RecE and RecT enhances the frequencies of spontaneous and UV-induced illegitimate recombination and that the RecJ, RecF, RecO, and RecR functions are required for this RecE-mediated illegitimate recombination. Moreover, we have also indicated that RecQ plays a role in the suppression of RecEmediated illegitimate recombination, with the participation of DnaB, Fis, Exol, and H-NS. Models have been proposed for these modes of recombination: the DNA gyrase subunit exchange model for short homology-independent illegitimate recombination and the "double-strand break and join" model for short homologydependent illegitimate recombination. Many features of these models remain to be tested in future studies.

在大肠杆菌lambda c1857溶原的诱导过程中,利用lamdabio转导噬菌体实验测量了非法重组的频率。非法重组分为短同源非依赖性非法重组和短同源依赖性非法重组两类。前者涉及几乎没有同源性的序列,由DNA拓扑异构酶介导,由DNA结合蛋白HU控制。后者是由紫外线照射或其他DNA损伤剂诱导的,需要在重组位点上有短的同源区域,通常包含4到13个碱基对。研究表明,RecJ外切酶促进短同源依赖的非法重组,而RecQ解旋酶抑制这种重组。此外,我们已经证明,RecE和RecT的过表达增加了自发和紫外线诱导的非法重组的频率,并且RecJ, RecF, RecO和RecR功能是这种RecE介导的非法重组所必需的。此外,我们还指出,在DnaB、Fis、Exol和H-NS的参与下,RecQ在抑制remeediated非法重组中发挥作用。针对这些重组模式,人们提出了DNA旋切酶亚基交换模型和“双链断裂连接”模型。这些模型的许多特征仍有待在未来的研究中检验。
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引用次数: 0
Studies and perspectives of calponin in smooth muscle regulation and cancer gene therapy 钙钙蛋白在平滑肌调控和肿瘤基因治疗中的研究与展望
Pub Date : 2003-01-01 DOI: 10.1016/S0065-227X(03)80004-7
Katsuhito Takahashi, Hisako Yamamura
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引用次数: 13
Fertilization and development initiation in orthodox and unorthodox ways: From normal fertilization to cloning 正统与非正统方式的受精与发育起始:从正常受精到克隆
Pub Date : 2003-01-01 DOI: 10.1016/S0065-227X(03)80003-5
Ryuzo Yanagimachi
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引用次数: 19
17 Years with Mr. Miyazaki 与宫崎骏共事17年
Pub Date : 2003-01-01 DOI: 10.1016/S0065-227X(03)80008-4
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引用次数: 0
Contributor sketches 贡献者草图
Pub Date : 2003-01-01 DOI: 10.1016/S0065-227X(03)80005-9
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引用次数: 0
Suggestions to authors 给作者的建议
Pub Date : 2003-01-01 DOI: 10.1016/S0065-227X(03)80006-0
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引用次数: 0
期刊
Advances in Biophysics
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