Somatic Cell and Molecular Genetics最新文献

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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。
Somatic Cell and Molecular Genetics Pub Date : 1997-11-01 DOI: 10.1007/BF02673748
H L MacArthur, M L Agarwal, S Bacchetti
{"title":"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.","authors":"H L MacArthur,&nbsp;M L Agarwal,&nbsp;S Bacchetti","doi":"10.1007/BF02673748","DOIUrl":"https://doi.org/10.1007/BF02673748","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":21884,"journal":{"name":"Somatic Cell and Molecular Genetics","volume":"23 6","pages":"379-89"},"PeriodicalIF":0.0,"publicationDate":"1997-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02673748","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20580061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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。
Somatic Cell and Molecular Genetics Pub Date : 1997-11-01 DOI: 10.1007/BF02673747
P Johnstone, C Reifsteck, S Kohler, P Worland, S Olson, R E Moses
{"title":"Fanconi anemia group A and D cell lines respond normally to inhibitors of cell cycle regulation.","authors":"P Johnstone,&nbsp;C Reifsteck,&nbsp;S Kohler,&nbsp;P Worland,&nbsp;S Olson,&nbsp;R E Moses","doi":"10.1007/BF02673747","DOIUrl":"https://doi.org/10.1007/BF02673747","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":21884,"journal":{"name":"Somatic Cell and Molecular Genetics","volume":"23 6","pages":"371-7"},"PeriodicalIF":0.0,"publicationDate":"1997-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02673747","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20580060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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。
Somatic Cell and Molecular Genetics 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
{"title":"Exon trapping and sequence-based methods of gene finding in transcript mapping of human 4p16.3.","authors":"I Pribill,&nbsp;G T Barnes,&nbsp;J Chen,&nbsp;D Church,&nbsp;A Buckler,&nbsp;S Baxendale,&nbsp;G P Bates,&nbsp;H Lehrach,&nbsp;M J Gusella,&nbsp;M P Duyao,&nbsp;C M Ambrose,&nbsp;J F Gusella,&nbsp;M E MacDonald","doi":"10.1007/BF02673751","DOIUrl":"https://doi.org/10.1007/BF02673751","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":21884,"journal":{"name":"Somatic Cell and Molecular Genetics","volume":"23 6","pages":"413-27"},"PeriodicalIF":0.0,"publicationDate":"1997-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02673751","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20580064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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。
Somatic Cell and Molecular Genetics Pub Date : 1997-11-01 DOI: 10.1007/BF02673749
L Desiderato, M W Davey, A A Piper
{"title":"Demethylation of the human MDR1 5' region accompanies activation of P-glycoprotein expression in a HL60 multidrug resistant subline.","authors":"L Desiderato,&nbsp;M W Davey,&nbsp;A A Piper","doi":"10.1007/BF02673749","DOIUrl":"https://doi.org/10.1007/BF02673749","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":21884,"journal":{"name":"Somatic Cell and Molecular Genetics","volume":"23 6","pages":"391-400"},"PeriodicalIF":0.0,"publicationDate":"1997-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02673749","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20580062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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。
Somatic Cell and Molecular Genetics 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
{"title":"Detailed analysis of a 17q21 microdissection library by sequence bioinformatics and isolation of region-specific clones.","authors":"K L Bentley,&nbsp;W L Li,&nbsp;F O VannBerg,&nbsp;J Y Choi,&nbsp;J Yu,&nbsp;F T Kao,&nbsp;G Ruaño","doi":"10.1007/BF02674282","DOIUrl":"https://doi.org/10.1007/BF02674282","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":21884,"journal":{"name":"Somatic Cell and Molecular Genetics","volume":"23 5","pages":"353-65"},"PeriodicalIF":0.0,"publicationDate":"1997-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02674282","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20501199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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。
Somatic Cell and Molecular Genetics 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
{"title":"Applications of green fluorescent protein as a marker of retroviral vectors.","authors":"E S Kandel,&nbsp;B D Chang,&nbsp;B Schott,&nbsp;A A Shtil,&nbsp;A V Gudkov,&nbsp;I B Roninson","doi":"10.1007/BF02674280","DOIUrl":"https://doi.org/10.1007/BF02674280","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":21884,"journal":{"name":"Somatic Cell and Molecular Genetics","volume":"23 5","pages":"325-40"},"PeriodicalIF":0.0,"publicationDate":"1997-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02674280","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20467826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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。
Somatic Cell and Molecular Genetics Pub Date : 1997-09-01 DOI: 10.1007/BF02674283
J Yu, Y Shen, S Tong, F T Kao
{"title":"Assignment of three human markers in chromosome 21q11 to mouse chromosome 16.","authors":"J Yu,&nbsp;Y Shen,&nbsp;S Tong,&nbsp;F T Kao","doi":"10.1007/BF02674283","DOIUrl":"https://doi.org/10.1007/BF02674283","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":21884,"journal":{"name":"Somatic Cell and Molecular Genetics","volume":"23 5","pages":"367-70"},"PeriodicalIF":0.0,"publicationDate":"1997-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02674283","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20467828","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 1
Correction of the Bloom syndrome cellular phenotypes. Bloom综合征细胞表型的校正。
Somatic Cell and Molecular Genetics Pub Date : 1997-09-01 DOI: 10.1007/BF02674278
T Giesler, K Baker, B Zhang, L D McDaniel, R A Schultz
{"title":"Correction of the Bloom syndrome cellular phenotypes.","authors":"T Giesler,&nbsp;K Baker,&nbsp;B Zhang,&nbsp;L D McDaniel,&nbsp;R A Schultz","doi":"10.1007/BF02674278","DOIUrl":"https://doi.org/10.1007/BF02674278","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":21884,"journal":{"name":"Somatic Cell and Molecular Genetics","volume":"23 5","pages":"303-12"},"PeriodicalIF":0.0,"publicationDate":"1997-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02674278","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20469230","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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。
Somatic Cell and Molecular Genetics Pub Date : 1997-09-01 DOI: 10.1007/BF02674279
S Tateishi, M Yamaizumi
{"title":"Cell cycle control is aberrant in Chinese hamster ovary cell mutants exhibiting apoptosis after serum deprivation.","authors":"S Tateishi,&nbsp;M Yamaizumi","doi":"10.1007/BF02674279","DOIUrl":"https://doi.org/10.1007/BF02674279","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":21884,"journal":{"name":"Somatic Cell and Molecular Genetics","volume":"23 5","pages":"313-23"},"PeriodicalIF":0.0,"publicationDate":"1997-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02674279","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20469231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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。
Somatic Cell and Molecular Genetics Pub Date : 1997-09-01 DOI: 10.1007/BF02674281
Y Ejima, M S Sasaki
{"title":"Phenotypic correction of ataxia-telangiectasia cellular defect by exogenously introduced human or mouse subchromosomal fragments.","authors":"Y Ejima,&nbsp;M S Sasaki","doi":"10.1007/BF02674281","DOIUrl":"https://doi.org/10.1007/BF02674281","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":21884,"journal":{"name":"Somatic Cell and Molecular Genetics","volume":"23 5","pages":"341-51"},"PeriodicalIF":0.0,"publicationDate":"1997-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF02674281","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20467827","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 2
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