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Induction of fragility at the human RNU2 locus by cytosine arabinoside is dependent upon a transcriptionally competent U2 small nuclear RNA gene and the expression of p53. 阿拉伯糖胞嘧啶诱导人类RNU2位点的易碎性依赖于具有转录能力的U2小核RNA基因和p53的表达。
Pub Date : 1997-11-01 DOI: 10.1007/BF02673748
H L MacArthur, M L Agarwal, S Bacchetti

Chromosomal fragile sites are regions that are intrinsically unstable and are susceptible to experimentally induced damage. In most cases, the target and mechanism of induction of fragility are unknown. Using ectopic integration of engineered DNA arrays to create "new" fragile sites, we and others have previously shown that the transcriptionally competent U2 gene is necessary and sufficient for induction of fragility at the RNU2 locus upon infection of human cells with Adenovirus 12. In the present study we have investigated the response of the RNU2 locus to cytosine arabinoside (araC), an inhibitor of DNA polymerases and a common inducer of fragile sites. We demonstrate that the RNU2 locus is sensitive to the drug and that araC-induced fragility is dependent upon a functional U2 gene and on the expression of the cellular p53 protein. Our results identify a novel DNA structure associated with fragile sites and suggest a role for transcription and repair processes in RNU2 fragility.

染色体脆弱位点是本质上不稳定的区域,容易受到实验诱导的损伤。在大多数情况下,脆弱性诱发的目标和机制是未知的。利用工程DNA阵列的异位整合来创建“新的”脆弱位点,我们和其他人之前已经证明,在腺病毒12感染人类细胞时,转录能力强的U2基因是诱导RNU2位点脆弱的必要和充分条件。在本研究中,我们研究了RNU2基因座对阿拉伯糖胞嘧啶(araC)的反应,araC是一种DNA聚合酶抑制剂和脆弱位点的常见诱导剂。我们证明RNU2位点对药物敏感,arac诱导的脆性依赖于功能U2基因和细胞p53蛋白的表达。我们的研究结果确定了一种与脆性位点相关的新型DNA结构,并提出了RNU2脆性中转录和修复过程的作用。
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引用次数: 6
Fanconi anemia group A and D cell lines respond normally to inhibitors of cell cycle regulation. 范可尼贫血A组和D组细胞系对细胞周期调节抑制剂反应正常。
Pub Date : 1997-11-01 DOI: 10.1007/BF02673747
P Johnstone, C Reifsteck, S Kohler, P Worland, S Olson, R E Moses

Cells from patients with Fanconi anemia (FA) show decreased viability and decreased chromosome stability after treatment with DNA cross-linking agents, compared to normal cells. FA cells also show a relative accumulation at the G2/M transition after such treatment. This has suggested a possible checkpoint abnormality. In the studies presented here, treatment with hydroxyurea, caffeine or inhibitors of cell cycle kinases did not reveal abnormalities in survival or chromosome stability in FA-A or FA-D cells. Chromosomal breaks introduced by hydrogen peroxide or methyl methanesulfonate accumulated to the same extent in FA-A or FA-D cells as in normal cells. We conclude that FA-A and FA-D cells respond normally to agents known to alter the cell cycle or introduce DNA strand breaks. FA cells process strand breaks and a variety of DNA monoadducts normally. Our results are compatible with repair of DNA crosslinks being slower in FA than in normal cells and FA cells having normal cell cycle checkpoints.

与正常细胞相比,范可尼贫血(FA)患者的细胞在DNA交联剂治疗后表现出活力下降和染色体稳定性下降。在此处理后,FA细胞在G2/M过渡阶段也显示出相对的积累。这表明可能存在检查点异常。在这里的研究中,用羟基脲、咖啡因或细胞周期激酶抑制剂治疗并没有显示FA-A或FA-D细胞的存活或染色体稳定性异常。过氧化氢或甲磺酸甲酯引起的染色体断裂在FA-A或FA-D细胞中积累的程度与正常细胞相同。我们得出结论,FA-A和FA-D细胞对已知改变细胞周期或引入DNA链断裂的药物反应正常。FA细胞通常处理链断裂和多种DNA单加合物。我们的结果与FA细胞的DNA交联修复速度比正常细胞慢以及FA细胞具有正常的细胞周期检查点相一致。
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引用次数: 12
Exon trapping and sequence-based methods of gene finding in transcript mapping of human 4p16.3. 人类4p16.3转录本定位中的外显子捕获和基于序列的基因发现方法。
Pub Date : 1997-11-01 DOI: 10.1007/BF02673751
I Pribill, G T Barnes, J Chen, D Church, A Buckler, S Baxendale, G P Bates, H Lehrach, M J Gusella, M P Duyao, C M Ambrose, J F Gusella, M E MacDonald

We have applied exon amplification, GRAIL2 exon prediction and EST database searching to a 2 Mb segment of chromosome 4p16.3. Experimental and computational methods of identifying exons were comparable in efficiency and apparent false positive rate, but were complementary in gene identification, revealing distinct overlapping sets of expressed sequences. EST searching was most powerful when we considered only those ESTs that show evidence of splicing relative to the genomic sequence. The combination of the three gene finding methods produced a transcription map of 30 loci in this segment of 4p16.3 that includes known human genes, homologs of loci identified in rodents and several anonymous transcripts, including a putative novel DNA polymerase and a gene related to Drosophila ash1. While most of the genes in the region have been found, our data suggest that even with the entire DNA sequence available, complete saturation of the transcript map will require additional, focused experimental effort.

我们利用外显子扩增、GRAIL2外显子预测和EST数据库搜索对染色体4p16.3的2mb片段进行了分析。外显子识别的实验方法和计算方法在效率和表观假阳性率方面具有可比性,但在基因识别方面具有互补性,揭示了不同的重叠表达序列集。当我们只考虑那些显示与基因组序列相关的剪接证据的EST时,EST搜索是最强大的。三种基因发现方法的结合产生了4p16.3片段30个位点的转录图谱,其中包括已知的人类基因,在啮齿动物中发现的同源基因和几个匿名转录本,包括假定的新型DNA聚合酶和与果蝇ash1相关的基因。虽然该区域的大多数基因已经被发现,但我们的数据表明,即使有了完整的DNA序列,转录图谱的完全饱和也需要额外的、集中的实验努力。
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引用次数: 5
Demethylation of the human MDR1 5' region accompanies activation of P-glycoprotein expression in a HL60 multidrug resistant subline. 在HL60多药耐药亚系中,人mdr15 '区的去甲基化伴随着p -糖蛋白表达的激活。
Pub Date : 1997-11-01 DOI: 10.1007/BF02673749
L Desiderato, M W Davey, A A Piper

Chemotherapy is frequently limited by the development of multidrug resistance, a major cause of which is activation of the P-glycoprotein-encoding MDR1 gene. We have previously developed a P-glycoprotein-expressing multidrug resistant subline (HL60/E8) from the non-P-glycoprotein-expressing human HL60 promyelocytic leukemia cell line. A possible cause of MDR1 silencing in HL60 cells is methylation of the promoter proximal region, thus demethylation occurring as a result of drug treatment may be responsible for MDR1 activation in the multidrug resistant subline. Using the bisulphite genomic sequencing technique we demonstrated that HL60 DNA is methylated at multiple sites within two distinct areas, one upstream and one downstream of the transcription start point. Only a single site in each area was methylated in all strands examined, with the remaining adjacent sites showing partial methylation. In contrast, DNA from the multidrug resistant HL60/E8 subline was unmethylated at essentially all sites in both areas. Thus the development of the P-glycoprotein-expressing multidrug resistant subline was associated with demethylation of the MDR1 5' region.

化疗经常受到多药耐药的限制,其中一个主要原因是p -糖蛋白编码MDR1基因的激活。我们之前从不表达p糖蛋白的人早幼粒细胞白血病细胞系中开发了一种表达p糖蛋白的多药耐药亚群(HL60/E8)。HL60细胞中MDR1沉默的一个可能原因是启动子近端区域的甲基化,因此药物治疗导致的去甲基化可能是多重耐药亚系中MDR1激活的原因。使用亚硫酸盐基因组测序技术,我们证明了HL60 DNA在转录起点的上游和下游两个不同区域的多个位点甲基化。在所有检测的链中,每个区域只有一个位点被甲基化,其余邻近位点显示部分甲基化。相比之下,来自多药耐药的HL60/E8亚系的DNA在两个区域的几乎所有位点都未甲基化。因此,表达p糖蛋白的多药耐药亚群的发展与mdr15 '区的去甲基化有关。
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引用次数: 45
Detailed analysis of a 17q21 microdissection library by sequence bioinformatics and isolation of region-specific clones. 利用序列生物信息学和区域特异性克隆分离技术对17q21微解剖文库进行详细分析。
Pub Date : 1997-09-01 DOI: 10.1007/BF02674282
K L Bentley, W L Li, F O VannBerg, J Y Choi, J Yu, F T Kao, G Ruaño

A region-specific microdissection library originating from human chromosome 17q21, was constructed using the MboI linker-adaptor microcloning technique. DNA sequencing of 241 microclones resulted in the identification of 74 novel coding sequences, paralogs of known genes, and known, but previously unmapped, genes or expressed sequence tags that were "virtually" mapped to chromosome 17q21. By pooling the microclones as multiplexed hybridization probes, and by virtue of their origin on 17q21, we were able to identify approximately 150 P1 clones from the human Reference Library Data Base P1 Library that potentially map to chromosome 17q21. Verification of the 17q21 location of 16 P1 clones was accomplished by PCR analysis with STS primer pairs to known 17q21 genes or by FISH. Our results demonstrate the substantial advantage of combining the sequence analysis of microclones with multiplex hybridization strategies for gene discovery and mapping specific gene rich regions of the genome.

利用MboI连接接头微克隆技术,构建了人类染色体17q21的区域特异性微解剖文库。241个微克隆的DNA测序结果鉴定出74个新的编码序列,已知基因的类似物,以及已知的,但以前未定位的基因或表达的序列标签,这些序列“实际上”定位到染色体17q21上。通过将这些微克隆作为多路杂交探针,并利用它们在17q21上的起源,我们能够从人类参考文库数据库P1文库中鉴定出大约150个可能定位于17q21染色体的P1克隆。用已知17q21基因的STS引物对进行PCR或FISH分析,验证了16个P1克隆的17q21位置。我们的研究结果表明,将微克隆序列分析与多重杂交策略相结合,在基因发现和基因组特定基因丰富区域定位方面具有巨大优势。
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引用次数: 1
Applications of green fluorescent protein as a marker of retroviral vectors. 绿色荧光蛋白作为逆转录病毒载体标记物的应用。
Pub Date : 1997-09-01 DOI: 10.1007/BF02674280
E S Kandel, B D Chang, B Schott, A A Shtil, A V Gudkov, I B Roninson

The Green Fluorescent Protein (GFP) of Aequorea victoria is used as a vital fluorescent tag for the detection and isolation of genetically modified cells. Several modified variants of GFP were tested as marker genes in retroviral vectors containing different backbones and promoter combinations. Constructs allowing for reliable detection of GFP fluorescence and the expression of a cotransduced gene from a strong promoter were identified. Cells harboring such constructs are detectable by flow cytometry, fluorescence microscopy and multi-well fluorescence reading. GFP expression in transduced cells is stable both in vitro and in vivo, and long-term dynamics of GFP-positive fractions in a mixed population can be used to monitor the biological effects of a cotransduced gene. Selection of cells with the highest GFP fluorescence enriches for multiply infected cells. The use of different GFP variants allows one to monitor simultaneously two cell populations transduced with vectors carrying GFPs that differ in their fluorescence intensity or spectral properties and to identify doubly transduced cells. In addition, transcription of an inducible promoter positioned in the opposite orientation to GFP can be monitored by the inhibition of GFP fluorescence. Thus, GFP provides a useful marker for gene transfer by retroviral vectors and extends the range of applications for retroviral transduction.

维多利亚Aequorea victoria的绿色荧光蛋白(Green Fluorescent Protein, GFP)是检测和分离转基因细胞的重要荧光标记。在含有不同主干和启动子组合的逆转录病毒载体中测试了几种GFP修饰变体作为标记基因。构建允许可靠的检测GFP荧光和强启动子共转导基因的表达。含有这种结构的细胞可以通过流式细胞术、荧光显微镜和多孔荧光读数检测到。GFP在转导细胞中的表达在体外和体内都是稳定的,并且在混合群体中GFP阳性组分的长期动态可用于监测共转导基因的生物学效应。选择具有最高GFP荧光的细胞可使感染细胞增殖。使用不同的GFP变体可以同时监测两个细胞群,这些细胞群被携带荧光强度或光谱特性不同的GFP的载体转导,并识别双重转导的细胞。此外,定位于与GFP相反方向的诱导启动子的转录可以通过抑制GFP荧光来监测。因此,GFP为逆转录病毒载体的基因转移提供了一个有用的标记,并扩展了逆转录病毒转导的应用范围。
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引用次数: 34
Assignment of three human markers in chromosome 21q11 to mouse chromosome 16. 人类21q11染色体上的三个标记在小鼠16号染色体上的定位。
Pub Date : 1997-09-01 DOI: 10.1007/BF02674283
J Yu, Y Shen, S Tong, F T Kao

Three unique sequence microclones from human chromosome region 21q11 were assigned to mouse chromosome 16 using a mouse/Chinese hamster cell hybrid 96Az2 containing a single mouse chromosome 16. This comparative mapping provides further homology between human chromosome 21 and mouse chromosome 16 to include the very proximal portion of the long arm of human chromosome 21. Since this part of human chromosome 21 is associated with mental retardation in Down syndrome individuals, its homologous mouse region should also be included in the construction of mouse models for studying Down syndrome phenotypes including mental retardation.

利用小鼠/中国仓鼠细胞杂交96Az2,将人类染色体21q11区的3个独特序列微克隆分配到小鼠16号染色体上。这一比较图谱进一步提供了人类21号染色体和小鼠16号染色体之间的同源性,包括人类21号染色体长臂的非常近端部分。由于人类21号染色体的这一部分与唐氏综合征个体的智力发育迟缓有关,因此在构建研究包括智力发育迟缓在内的唐氏综合征表型的小鼠模型时,也应纳入其小鼠同源区域。
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引用次数: 1
Correction of the Bloom syndrome cellular phenotypes. Bloom综合征细胞表型的校正。
Pub Date : 1997-09-01 DOI: 10.1007/BF02674278
T Giesler, K Baker, B Zhang, L D McDaniel, R A Schultz

Bloom syndrome (BLM) is a genetic disorder associated with predisposition to cancer and chromosome instability. However, the most readily recognized clinical feature of the syndrome is growth retardation. Introduction of the previously cloned BLM gene into BLM cells yielded correction of the chromosome instability and slow growth phenotypes. Additionally, asynchronous cultures of complemented clones revealed a lower percentage of cells in S-phase than uncomplemented BLM cells. These results support the notion that BLM is a defect in which short stature, chromosome instability and cancer predisposition are all associated with an error in DNA replication.

布卢姆综合征(BLM)是一种与癌症易感性和染色体不稳定相关的遗传疾病。然而,该综合征最容易识别的临床特征是生长迟缓。将先前克隆的BLM基因导入BLM细胞,纠正了染色体不稳定和生长缓慢的表型。此外,互补克隆的异步培养显示s期细胞比例低于未互补的BLM细胞。这些结果支持了这样一种观点,即BLM是一种缺陷,其中身材矮小、染色体不稳定和癌症易感性都与DNA复制错误有关。
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引用次数: 6
Cell cycle control is aberrant in Chinese hamster ovary cell mutants exhibiting apoptosis after serum deprivation. 中国仓鼠卵巢细胞突变体在血清剥夺后出现细胞凋亡,细胞周期控制异常。
Pub Date : 1997-09-01 DOI: 10.1007/BF02674279
S Tateishi, M Yamaizumi

We isolated mutants of Chinese hamster ovary cells that exhibit excessive apoptosis after serum deprivation. In the medium containing 10% serum, the growth rates of the mutants were 1.4 to 1.5-fold faster than those of wild-type cells. Whereas the cell cycle of wild-type cells was arrested at the G1 phase after serum deprivation, the cell cycle of the mutant cells was not fully arrested at this phase, suggesting that cell cycle regulation was disorganized in the mutants. The mutants were highly sensitive to a nucleotide-analogue 5-fluorouracil in the absence of serum, whereas wild-type cells were resistant to the drug. Based on the sensitivity to the drug after serum deprivation, we could classify the mutants into dominant groups and at least two recessive complementation groups. Thus, these mutants presumably contain different lesions in gene(s) required for cell cycle regulation and apoptosis.

我们分离了中国仓鼠卵巢细胞在血清剥夺后过度凋亡的突变体。在含10%血清的培养基中,突变体的生长速度比野生型细胞快1.4 ~ 1.5倍。血清剥夺后,野生型细胞的细胞周期被阻滞在G1期,而突变型细胞的细胞周期并没有完全阻滞在G1期,这表明突变体的细胞周期调节是紊乱的。在没有血清的情况下,突变体对核苷酸类似物5-氟尿嘧啶高度敏感,而野生型细胞对该药物具有耐药性。根据血清剥夺后对药物的敏感性,我们可以将突变体分为显性组和至少两个隐性互补组。因此,这些突变体可能在细胞周期调控和细胞凋亡所需的基因中含有不同的损伤。
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引用次数: 2
Phenotypic correction of ataxia-telangiectasia cellular defect by exogenously introduced human or mouse subchromosomal fragments. 外源性引入人或小鼠亚染色体片段对共济失调-毛细血管扩张细胞缺陷的表型校正。
Pub Date : 1997-09-01 DOI: 10.1007/BF02674281
Y Ejima, M S Sasaki

A human-mouse hybrid containing a human 11q22-23 fragment including the ATM locus was used to examine its capability to correct the cellular defect of ataxia-telangiectasia (A-T). Examination of 21 A-T-derived hybrids indicated that the acquired radioresistance was observed in the clones where the 11q22-23 fragment was transferred intact, but not in those where donor-derived 11q segment was lost. In one exceptional clone, the ATM locus was deleted from the transferred fragment, while it was still partially radioresistant. This partially radioresistant clone was found to include the mouse-derived fragment containing the Atm gene, the mouse homologue of human ATM gene. Similar association of partial radioresistance with the presence of mouse Atm gene was observed in three additional hybrids. The results indicate that the cellular A-T defect can be corrected by the mouse subchromosomal fragment containing the Atm gene as well as by the human 11q22-23 fragment containing the ATM gene, but apparently to a lesser extent in the former.

一个含有人类11q22-23片段(包括ATM位点)的人-鼠杂交体被用来检测其纠正共济失调-毛细血管扩张(A- t)细胞缺陷的能力。对21个a - t来源杂交种的检测表明,在11q22-23片段完整转移的克隆中观察到获得性辐射抗性,而在供体来源11q片段丢失的克隆中则没有。在一个例外的克隆中,ATM位点被从转移的片段中删除,而它仍然部分具有辐射抗性。这个部分耐辐射的克隆被发现包括含有Atm基因的小鼠来源片段,这是人类Atm基因的小鼠同源物。在另外三个杂交种中观察到部分辐射抗性与小鼠Atm基因的存在相似的关联。结果表明,含有Atm基因的小鼠亚染色体片段和含有Atm基因的人11q22-23片段都能纠正细胞a - t缺陷,但前者的纠正程度明显较弱。
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引用次数: 2
期刊
Somatic Cell and Molecular Genetics
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