摘要:

We have used a number of banding techniques to analyze the chromosomal content of two sublines of the steroid-secreting mouse adrenocortical tumor cell line Y1. One of the sublines contains marker chromosomes with large “homogeneously staining regions” (HSRs). The other subline contains numerous double minutes, but no HSR. The presence of marker chromosomes shared by both sublines indicates their derivation from a common precursor. Both sublines are karyotypically stable, have similar growth rates, and exhibit positive staining for Δ5,3β-Hydroxysteroid dehydrog

ISSN:1424-8581    

DOI:10.1159/000131535

出版商:S. Karger AG    

年代:1980

数据来源: Karger

摘要:

Ouabain resistant mutants of hypoxanthine phosphoribosyl transferase deficient HeLa cells and euploid human fibroblasts were isolated and extensively characterized. These double mutants were used to test the prediction that they would be “universal hybridizers” for intraspecific human cell hybrid production. Hybrids were selected from fusions with human cells of diverse somatic origin. In addition it was shown that multi-parental hybrids can be generated using a modification of the selection system, a result which will be useful for gene dosage experiments involving human ce

ISSN:1424-8581    

DOI:10.1159/000131536

出版商:S. Karger AG    

年代:1980

数据来源: Karger

摘要:

A total of 1,319 chromosomal breaks and rearrangements, induced in human lymphocytes by mitomycin C, was investigated. Patterns of “preference” and “avoidance” among the partners of chromosomal rearrangements were easily discerned. The centromeric regions of chromosomes 1, 9, and 16 were most frequently involved in rearrangements that tended to occur between homologs. The acrocentric chromosomes prefer rearrangements within their own group, including homologs, and avoid involvement with the centromeric region of chromosome No. 9 (9c). Regions designated as “rarely rearranging” avoid the centromeres of 1 and 9 and prefer rearrangements within their own groups. No correlation could be demonstrated between the frequency of open breaks and rearrangements in the same chromos

ISSN:1424-8581    

DOI:10.1159/000131537

出版商:S. Karger AG    

年代:1980

数据来源: Karger

摘要:

The in vivo genomic mutagenicity of colchicine in Chinese hamster primary oocytes was analyzed at a carefully chosen dose that did not completely arrest the formation of the first meiotic spindle but exhibited a remarkable ability to induce nondisjunction, very possibly as a result of inhibition of tubulin polymerization. A single dose of 3 µg of colchicine per gram body weight was administered intraperitoneally at the onset of formation of the first meiotic spindle in females with a normal estrous cycle. Morphologically abnormal secondary oocytes with one or two extremely large first polar bodies occurred frequently, namely, in 47 (11.3%) of 416 oocytes. Chromosome analysis of a total of 2,124 secondary oocytes revealed that the overall incidence of aneuploids increased significantly (P < 0.001) in the experimental group (25.9%, or 99/382) as compared with the control group (2.0%, or 35/1,742). The minimum genomic mutagenicity of colchicine caused non-disjunction in one or two bivalents and eventually induced the formation of aneuploid secondary oocytes with chromosome numbers within the haploid range. The maximum genomic mutagenicity at the selected dose caused the elimination of a large number of chromosomes from the egg body, in association with the formation of a giant polar body or bodies. Three types, each with two subdivisions, of abnormal chromosome segregation between the oocytes and their giant polar body or bodies were studied, revealing part of the process resulting in aneuploid production due to either nondisjunction or anaphase lagging. The fate of the lagging chromosomes was also observed; they were included in neither the oocytes nor the polar body but eventually degenerated within the perivitelline space. The conditions of the spindle in oocytes aged by pre- and postovulatory over-ripeness, both of which have been known to induce meiotic chromosomal nondisjunction, are discussed in relation to tubulin polymerization

ISSN:1424-8581    

DOI:10.1159/000131538

出版商:S. Karger AG    

年代:1980

数据来源: Karger

摘要:

In a diploid fibroblast culture from a patient with Fanconi anemia (FA), we observed the evolution of a chromosomally abnormal clone that had an unusual proliferative advantage and increased growth potential compared with the diploid FA cells. Q-, G-, C-, and Ag-NOR banding analyses revealed that the clonal cells had the chromosomal complement 46, XY, –5,-21, + marl,+mar2, and were trisomic for a segment of the long arm of chromosome 5 and most of the long arm of No. 21. The retention of chromosome instability in the clonal cells indicates that the alteration in growth characteristics did not result from a mutation to the wild-type allele at the FA locu

ISSN:1424-8581    

DOI:10.1159/000131539

出版商:S. Karger AG    

年代:1980

数据来源: Karger

摘要:

Evidence is presented indicating that human chromosome 11 carries a structural locus for fibronectin (FN). A panel of cell hybrids of FN fiber-producing normal human diploid cells fused with mouse A9 cells were immunofluorescently stained with species-specific, affinity purified antibodies to human FN (AHFN); similar anti-mouse FN antibodies (AMFN); and the nonspecies-specific anti-FN antiserum (AFN) which was used in an earlier study of this same hybrid panel (Eun and Klinger, 1980). All hybrids that had the human 11 produced extracellular fibers that fluoresced brightly when reacted with the AHFN and AFN. All other human chromosomes could be eliminated as being related to FN production, suggesting that the 11 carries a structural FN locus. This agrees with our earlier study in which a nonspecies-specific antiserum was used and with the preliminary report of Smith et al. (1979), who used a different cell system. The apparent discrepancy between these results and those of Owerbach et al. (1978), who reported synteny of FN with the human No. 8, was partly resolved in that one of their FN positive hybrids was found to react with our AMFN but not with the AHFN, suggesting that some other as yet undefined mechanism may be operating in their hybrids which were made with mouse LM/TK cells. The parental mouse A9 cells of our hybrids do not produce FN fibers, although a radioimmunoassay detects a small amount of mouse FN secreted into the medium. The fibers of some of our AHFN positive hybrids also react weakly with AMFN, but none react only with AMFN. This suggests that fibers produced by these hybrids bind some mouse as well as human FN. Why this is not so in all the producers is not clear.

ISSN:1424-8581    

DOI:10.1159/000131540

出版商:S. Karger AG    

年代:1980

数据来源: Karger

ISSN:1424-8581    

DOI:10.1159/000131541

出版商:S. Karger AG    

年代:1980

数据来源: Karger

ISSN:1424-8581    

DOI:10.1159/000131542

出版商:S. Karger AG    

年代:1980

数据来源: Karger

ISSN:1424-8581    

DOI:10.1159/000131543

出版商:S. Karger AG    

年代:1980

数据来源: Karger

ISSN:1424-8581    

DOI:10.1159/000131544

出版商:S. Karger AG    

年代:1980

数据来源: Karger