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Aedes albopictus cells resistant to adenosine because of a defect in nucleoside transport. 白纹伊蚊细胞因核苷转运缺陷而对腺苷产生抗性。
Somatic Cell Genetics Pub Date : 1982-09-01 DOI: 10.1007/BF01542852
A Sherwood, V Stollar
{"title":"Aedes albopictus cells resistant to adenosine because of a defect in nucleoside transport.","authors":"A Sherwood,&nbsp;V Stollar","doi":"10.1007/BF01542852","DOIUrl":"https://doi.org/10.1007/BF01542852","url":null,"abstract":"<p><p>By growing Aedes albopictus mosquito cells in media containing increasing concentrations of adenosine and subsequently plating low numbers of cells in the presence of EHNA (an inhibitor of adenosine deaminase), three clones were obtained which were resistant to adenosine. The adenosine-resistant clones contained level of adenosine and thymidine kinase similar to those in the parental cells, but were unable to incorporate labeled nucleotides (adenosine, uridine, thymidine, or guanosine) into TCA-precipitable material. The inability to incorporate nucleosides was also reflected in an enhanced resistance to several nucleoside analogs such as 5-fluorodeoxyuridine and tubercidin but not to the unribosylated base, 5-fluorouracil. Direct measurements over short time intervals indicated that the primary defect in these cells was at the level of nucleoside transport.</p>","PeriodicalId":21767,"journal":{"name":"Somatic Cell Genetics","volume":"8 5","pages":"575-85"},"PeriodicalIF":0.0,"publicationDate":"1982-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01542852","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18151021","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: 10
Gene for glutathione S-transferase-1 (GST1) is on human chromosome 11. 谷胱甘肽s -转移酶1 (GST1)基因位于人类第11号染色体上。
Somatic Cell Genetics Pub Date : 1982-09-01 DOI: 10.1007/BF01542859
D L Silberstein, T B Shows
{"title":"Gene for glutathione S-transferase-1 (GST1) is on human chromosome 11.","authors":"D L Silberstein,&nbsp;T B Shows","doi":"10.1007/BF01542859","DOIUrl":"https://doi.org/10.1007/BF01542859","url":null,"abstract":"<p><p>The glutathione S-transferases (GST) are a group of related enzymes that can detoxify potentially carcinogenic electrophiles by conjugating them with reduced glutathione (GSH). The chromosomal location of one of the enzyme forms, GST1, reported recently to be polymorphic, was determined utilizing man-mouse somatic cell hybrids segregating human chromosomes. The expression of GST1 by hybrid clones was compared with that of 34 enzyme markers representing 23 chromosomes, and karyotypes of selected cell hybrids were analyzed. The evidence indicated that GST1 is assigned to chromosome 11 in humans. Utilizing and X/11 translocation segregating in hybrids, GST1 was localized to the p13 leads to qter region of chromosome 11.</p>","PeriodicalId":21767,"journal":{"name":"Somatic Cell Genetics","volume":"8 5","pages":"667-75"},"PeriodicalIF":0.0,"publicationDate":"1982-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01542859","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18007532","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: 16
Genetic analysis of tumorigenesis: X. Chromosome studies of transformed mutants and tumor-derived CHEF/18 cells. 肿瘤发生的遗传分析:x。转化突变体和肿瘤来源的CHEF/18细胞的染色体研究。
Somatic Cell Genetics Pub Date : 1982-09-01 DOI: 10.1007/BF01542860
R M Kitchin, I K Gadi, B L Smith, R Sager
{"title":"Genetic analysis of tumorigenesis: X. Chromosome studies of transformed mutants and tumor-derived CHEF/18 cells.","authors":"R M Kitchin,&nbsp;I K Gadi,&nbsp;B L Smith,&nbsp;R Sager","doi":"10.1007/BF01542860","DOIUrl":"https://doi.org/10.1007/BF01542860","url":null,"abstract":"<p><p>Chinese hamster embryo fibroblast cell line CHEF/18 is stably diploid, anchorage-dependent, has a high serum requirement, and a does not form tumors in nude mice. The chromosome constitutions of spontaneous and chemically induced anchorage-independent and/or low-serum CHEF/18 mutants and tumors produced in nude mice by some of these mutants are compared. We find a correlation between diploidy and nontumorigenicity among the anchorage-independent mutants but not in the low-serum mutants. One of the four spontaneous and six of the 15 chemically induced anchorage mutants have remained diploid. The remaining 12 mutants are pseudodiploid or aneuploid, and seven of them contain changes in chromosome 1, either a translocation or a deletion involving breakage at the same position (1q11-12). Each of the tumors induced by six mutants has a unique pattern of rearrangements; however five of the six have changes involving chromosome 3. This chromosome was also frequency rearranged in tumor-derived cells previously investigated.</p>","PeriodicalId":21767,"journal":{"name":"Somatic Cell Genetics","volume":"8 5","pages":"677-89"},"PeriodicalIF":0.0,"publicationDate":"1982-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01542860","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18150920","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: 20
Induction of supermelanin synthesis and morphological changes in interspecific reconstituted cells and its reversal by tumor promoter. 肿瘤启动子诱导种间重组细胞超黑色素合成和形态改变及其逆转。
Somatic Cell Genetics Pub Date : 1982-09-01 DOI: 10.1007/BF01542854
T Sekiguchi, M Tosu, M C Yoshida, A Oikawa, K Ishihara, H Fujiki, M Tumuraya, T Kameya
{"title":"Induction of supermelanin synthesis and morphological changes in interspecific reconstituted cells and its reversal by tumor promoter.","authors":"T Sekiguchi,&nbsp;M Tosu,&nbsp;M C Yoshida,&nbsp;A Oikawa,&nbsp;K Ishihara,&nbsp;H Fujiki,&nbsp;M Tumuraya,&nbsp;T Kameya","doi":"10.1007/BF01542854","DOIUrl":"https://doi.org/10.1007/BF01542854","url":null,"abstract":"<p><p>Chloramphenicol-resistant (CAPr) reconstituted cells and cybrids were isolated by fusion of karyoplasts (or intact cells) of mouse amelanotic melanoma B16 cells with cytoplasts of hypoxanthine-guanine phosphoribosyltransferase (HGPRT) -deficient, CAPr rat myoblastic cells, L6TG.CAPr, and double selection in HAT medium containing CAP. Reconstituted cells or cybrids exhibited unique cellular arrangement, and about one third of the isolated clones expressed high tyrosinase activity and marked melanin synthesis, although the parental mouse cells expressed low tyrosinase activity and the parental rat cells did not express tyrosinase activity. These phenotypic changes have been stable for more than a year. The phenotypic reversions of these clonal cells were induced by treatment with a tumor promoter. There were changes in the morphology of the treated cells to that of the mouse B16 cells and extinction of tyrosinase activity and melanin synthesis in pigmented clonal cells. These phenotypic changes and reversions induced by a promoter were repeatedly reversible.</p>","PeriodicalId":21767,"journal":{"name":"Somatic Cell Genetics","volume":"8 5","pages":"605-22"},"PeriodicalIF":0.0,"publicationDate":"1982-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01542854","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17866206","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: 17
Isolation of Chinese hamster ovary cells with reduced unscheduled DNA synthesis after UV irradiation. 紫外光照射后中国仓鼠卵巢细胞非预定DNA合成减少的分离。
Somatic Cell Genetics Pub Date : 1982-09-01 DOI: 10.1007/BF01542856
M Stefanini, A Reuser, D Bootsma
{"title":"Isolation of Chinese hamster ovary cells with reduced unscheduled DNA synthesis after UV irradiation.","authors":"M Stefanini,&nbsp;A Reuser,&nbsp;D Bootsma","doi":"10.1007/BF01542856","DOIUrl":"https://doi.org/10.1007/BF01542856","url":null,"abstract":"<p><p>A simple procedure has been worked out to obtain UV-sensitive mutants of Chinese hamster ovary (CHO) cells. In this procedure, conventional mutagenesis is followed by BrdU--light treatment to enrich the population for UV-sensitive cells. Colonies that are allowed to form subsequently are duplicated by replica plating and screened on the master plate for their UV sensitivity and their capacity to carry out UV-induced DNA repair synthesis. Putative mutants are isolated from the replica. With this combination of methods, we succeeded in isolating CHO mutants with an 85-95% reduced level of UV-induced DNA synthesis in combination with an increased UV sensitivity.</p>","PeriodicalId":21767,"journal":{"name":"Somatic Cell Genetics","volume":"8 5","pages":"635-42"},"PeriodicalIF":0.0,"publicationDate":"1982-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01542856","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18150918","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: 27
Studies on cell division in mammalian cells: VI. A temperature-sensitive mutant blocked in both G1 and G2 phases of the cell cycle. 哺乳动物细胞分裂的研究:六。在细胞周期的G1和G2期被阻断的温度敏感突变体。
Somatic Cell Genetics Pub Date : 1982-09-01 DOI: 10.1007/BF01542858
D J Chen, R J Wang
{"title":"Studies on cell division in mammalian cells: VI. A temperature-sensitive mutant blocked in both G1 and G2 phases of the cell cycle.","authors":"D J Chen,&nbsp;R J Wang","doi":"10.1007/BF01542858","DOIUrl":"https://doi.org/10.1007/BF01542858","url":null,"abstract":"<p><p>A temperature-sensitive mammalian cell cycle mutant with blocks in G1 and G2 phases of the cell cycle has been isolated in culture. When shifted from the permissive temperature of 33 degrees C to the nonpermissive temperature of 39 degrees C, the fraction of cells initiating DNA synthesis as well as the fraction of cells entering mitosis decreased rapidly. Combined cytophotometric and autoradiographic analysis on the cells at 39 degrees C showed that G1 cells, with the exception of those in late G1, were arrested in that phase. Cells is S phase at the time of temperature shift, together with the late g1 cells which subsequently entered S, continued through S into G2, but were blocked in that phase of the cell cycle and unable to initiate mitosis. Those cells already in mitosis completed cell division at 39 degrees C. The G1 block point of ts-550C was found to be located after the serum starvation and isoleucine deprivation arrest points, approximately 3 h before initiation of DNA synthesis.</p>","PeriodicalId":21767,"journal":{"name":"Somatic Cell Genetics","volume":"8 5","pages":"653-66"},"PeriodicalIF":0.0,"publicationDate":"1982-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01542858","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"17248023","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: 11
Isolation of a spontaneous CHO amino acid transport mutant by a combination of tritium suicide and replica plating. 氚自杀与复刻相结合分离CHO氨基酸转运突变体。
Somatic Cell Genetics Pub Date : 1982-07-01 DOI: 10.1007/BF01538711
A H Dantzig, C W Slayman, E A Adelberg
{"title":"Isolation of a spontaneous CHO amino acid transport mutant by a combination of tritium suicide and replica plating.","authors":"A H Dantzig,&nbsp;C W Slayman,&nbsp;E A Adelberg","doi":"10.1007/BF01538711","DOIUrl":"https://doi.org/10.1007/BF01538711","url":null,"abstract":"<p><p>A spontaneous transport mutant of Chinese hamster ovary cells, CHY-1, was isolated by a combination of [3H]proline suicide and replica plating. The mutant took up less tritium than the parent, resulting in a lower killing rate during storage. Transport by four separate amino acid transport systems (A, ASC, L, Ly+) was examined. The CHY-1 mutant exhibited normal uptake via the ASC, L, and Ly+ systems. By contrast, uptake of the most specific substrate of the A system, 2-(methylamino)-isobutyric acid, was significantly reduced at low, but not high, concentrations, due to a 3.5-fold increase in Km and a 1.5-fold increase in Vmax. Taken together, these data suggest that the CHY-1 mutation may be in the structural gene coding for the A transport protein. The tritium suicide procedure is discussed, and general equations are derived to predict the maximum storage time for the survival of one mutant cell and the optimum size of the cell population for maximum mutant enrichment.</p>","PeriodicalId":21767,"journal":{"name":"Somatic Cell Genetics","volume":"8 4","pages":"509-20"},"PeriodicalIF":0.0,"publicationDate":"1982-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01538711","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18138934","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: 15
Isolation and characterization of puromycin-resistant clones from cultured mosquito cells. 蚊子培养细胞中抗嘌呤霉素克隆的分离与鉴定。
Somatic Cell Genetics Pub Date : 1982-07-01 DOI: 10.1007/BF01538712
A M Fallon, V Stollar
{"title":"Isolation and characterization of puromycin-resistant clones from cultured mosquito cells.","authors":"A M Fallon,&nbsp;V Stollar","doi":"10.1007/BF01538712","DOIUrl":"https://doi.org/10.1007/BF01538712","url":null,"abstract":"<p><p>We have isolated from an established Aedes albopictus (mosquito) cell line clones which are resistant to the antibiotic puromycin. On the basis of growth and plating efficiency, clones Pur-8026 and Pur-8612 were five- and seven-fold more resistant, respectively, to puromycin than wild-type cells. In vitro protein synthesis was resistant to puromycin only in extracts prepared from Pur-8612 cells. Measurements of puromycin transport, cross-resistance to colchicine, and sensitivity to Tween-80 indicating that resistance in Pur-8026 cells was due to membrane alteration(s) affecting permeability to puromycin. This is the first description of puromycin resistant in insect cells and also the first report of puromycin resistance in an animal cell variant associated with an alteration at the level of protein synthesis.</p>","PeriodicalId":21767,"journal":{"name":"Somatic Cell Genetics","volume":"8 4","pages":"521-32"},"PeriodicalIF":0.0,"publicationDate":"1982-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01538712","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18138935","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: 16
Isolation of deoxycoformycin-resistant cells with increased levels of adenosine deaminase. 腺苷脱氨酶水平升高的脱氧辅甲霉素耐药细胞的分离。
Somatic Cell Genetics Pub Date : 1982-07-01 DOI: 10.1007/BF01538708
P A Hoffee, S W Hunt, J Chiang
{"title":"Isolation of deoxycoformycin-resistant cells with increased levels of adenosine deaminase.","authors":"P A Hoffee,&nbsp;S W Hunt,&nbsp;J Chiang","doi":"10.1007/BF01538708","DOIUrl":"https://doi.org/10.1007/BF01538708","url":null,"abstract":"<p><p>Deoxycoformycin (dCF) is a specific inhibitor of adenosine deaminase (ADA). Rat hepatoma cells deficient in adenosine kinase and growing on adenosine as the sole carbon source are sensitive to the lethal action of dCF. Mutants resistant to dCF arise spontaneously with a frequency of 1.7 x 10(-6). This frequency is increased to 2.6 x 10(-5) by prior mutagenesis with ethyl methane sulfonate. Initially, dCF-resistant cell lines have 3-10 times the level of adenosine deaminase when compared to sensitive parental cells. Subsequent selection of mutants resistant to increased concentrations of dCF results in cells with a 15- to 30-fold increase in ADA levels. Quantitative immunoprecipitation tests indicate that the increase in enzyme activity in one line tested is due to an increase in the number of ADA molecules. These dCF' cell lines may serve as a model system to study the human disease state, hereditary hemolytic anemia, which is associated with increased levels of ADA.</p>","PeriodicalId":21767,"journal":{"name":"Somatic Cell Genetics","volume":"8 4","pages":"465-77"},"PeriodicalIF":0.0,"publicationDate":"1982-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01538708","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18029557","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
Serum protein synthesis by somatic cell hybrids. 体细胞杂交合成血清蛋白。
Somatic Cell Genetics Pub Date : 1982-07-01 DOI: 10.1007/BF01538706
L K Wray, H E Sutton
{"title":"Serum protein synthesis by somatic cell hybrids.","authors":"L K Wray,&nbsp;H E Sutton","doi":"10.1007/BF01538706","DOIUrl":"https://doi.org/10.1007/BF01538706","url":null,"abstract":"<p><p>Serum protein synthesis by rodent hepatomaa x fibroblast, hepatom a x teratocarcinoma, and hepatoma x hepatoma somatic cell hybrids was analyzed by Laurell (rocket) and crossed immunoelectrophoresis. With the hepatoma x fibroblast hybrids, of the nine serum proteins investigated, only transferrin was synthesized by the hybrids (with the exception of one hybrid clone which made albumin). Rat hepatoma (MHC) x mouse teratocarcinoma hybrids did not synthesize transferrin, but one of three clones did produce albumin. Rat hepatopma (Faza) x mouse hepatoma (Hepa 1) hybrids synthesized reduced amounts of albumin and transferrin, compared with the parental hepatoma cell lines. From these studies transferrin synthesis appears to be under different controls from the other serum proteins examined.</p>","PeriodicalId":21767,"journal":{"name":"Somatic Cell Genetics","volume":"8 4","pages":"433-49"},"PeriodicalIF":0.0,"publicationDate":"1982-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1007/BF01538706","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18138932","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
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