摘要:

The high chromosomal instability in New Zealand black mice was greatly reduced (to normal values) in vivo by repeated injections of bovine superoxide dismutase (Cu-SOD) over a period of 3 wk. The decrease in aberrations occurred in all the mice treated, and the SOD appeared to be effective for all types of aberrations, including chromatid gaps, telomeric constrictions, chromatid breaks, telomeric extrusions, and fragments.

ISSN:1424-8581    

DOI:10.1159/000131592

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

A pericentric inversion induced in a Robertsonian chromosome was recovered and analyzed in a male heterozygous for the rearrangement. Identification was made from chromosome banding and confirmed by synaptonemal complex (SC) analyses. From the former, the chromosome was identified as Rb4Bnr. The inversion involves about 34% of the chromosome length, and is designated In(11.13LS)29Rk. Analysis of SC inversion loops gave break points at 0.20 in the short arm and 0.54 in the long arm. Inhibition of homologous synapsis in the inversion was observed at zygotene and early pachytene, while synaptic adjustment was found to lead to heterologous SC formation at late pachytene. The inversion is believed to be causally related to the reduction in fertility observed in the carriers.

ISSN:1424-8581    

DOI:10.1159/000131593

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Patterns of DNA replication, fluorescence, and meiotic pairing have been studied in the composite X and Y chromosomes of a rodent, the soft-furred field rat, Millardia meltada. The heterochromatin of both the chromosomes replicates during late S and fluoresces brightly with Netropsin-Olivomycin. The fluorescence with Actinomycin D-Hoechst is dull, suggesting that the heterochromatin of both the X and the Y is relatively GC-rich. When surface-spread testis cells are analysed after silver staining considerable portions of the X and Y exhibit synapsis. On the basis of this study it appears that the heterochromatin of the X chromosome of M. meltada is substantially similar to that of the Y chromosome.

ISSN:1424-8581    

DOI:10.1159/000131594

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Chinese hamster × human and mouse × human somatic cell hybrid lines were obtained using circulating leucocytes from six chronic myeloid leukemia patients. All six patients carried the Ph1 translocation, t(9q+;22q–), characteristic of chronic myeloid leukemia, in their dividing immature granulocytes. Analysis of independent hybrid clones yielded the following results: 1. The chromosome 9 markers, soluble aconitase and adenylate kinase-1, segregated with the 9q+ derivative. The latter marker has previously been localized to 9q34. 2. The chromosome 22 markers, mitochondrial aconitase, N-acetyl-α-D-galactosaminidase, and arylsulfatase-A, also segregated with the 9q+ derivative. Mitochondrial aconitase has recently been assigned to 22q11→22q13. No evidence was obtained either for reciprocity of the translocation or for variations in breakpoints in different patients. The results reported in this paper provisionally assign the gene for mitochondrial aconitase to a region distal to the breakpoint in

ISSN:1424-8581    

DOI:10.1159/000131595

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Skin fibroblast-like (FL) cells from patients with Werner’s syndrome (adult progeria) regularly demonstrate frequent pseudodiploidy involving variable structural rearrangements that are clonal: variegated translocation mosaicism (VTM). Ninety-two percent of 1,538 metaphases from 29 independent strains derived from five patients with Werner’s syndrome demonstrated this cytogenetic abnormality. In contrast, only eight (8.4%) of 95 non-Werner’s syndrome FL cell cultures demonstrated VTM: seven with low-grade VTM (approximately 5% of 300 metaphases), and one with VTM affecting 90–100% of metaphases. Unlike the cytogenetic abnormalities observed in the terminal stages of normal FL cell cultures, VTM occurs throughout the entire lifespan of Werner’s syndrome cultures. Ten of the identifiable break points in 1,005 banded metaphases accounted for 27% of all definable rearrangements. Baseline sister chromatid exchanges were not increased. Co-cultivation of Werner’s syndrome and normal strains did not induce VTM in the normal strain. The relationship between VTM and the reduced growth potential of Werner’s syndrome FL cells is not yet understood, nor is the relationship between these in vitro abnormalities and the presumptive single gene defect that causes the progeroid clinical manifestations of Wern

ISSN:1424-8581    

DOI:10.1159/000131596

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

Skin fibroblast-like (FL) cells from patients with Werner’s syndrome (adult progeria) demonstrate multiple, stable, structural chromosome rearrangements (variegated translocation mosaicism) which can be used to identify cytogenetically marked clones of cells within a mass culture. We have cytogenetically followed eight FL cell strains (from two patients) throughout their entire in vitro replicative lifespans, and we show a correlation between the expansion and attenuation of individual clones and the growth of the mass cultures. One strain, which was aged several times, demonstrated a generally reproducible pattern of clonal succession but, surprisingly, also demonstrated, in two parallel derivative cultures, the late emergence of two relatively rapidly growing clones that had not been observed in the parental culture. These observations suggest that clonal succession and clonal attenuation occur in mass cultures, as had been predicted on the basis of dilute-plating cloning experiments. Our results may have implications for models of in vitro cellular senescence. In addition, there are interesting parallels with the tissue hyperplasia associated with in vivo aging, and this observation is compatible with the suggestion that skin FL cells in vitro provide a model for hyperplasia in viv

ISSN:1424-8581    

DOI:10.1159/000131597

出版商:S. Karger AG    

年代:1981

数据来源: Karger

摘要:

The role of guanine deaminase in selective cellular resistance to 8-azaguanine was examined, using eight mammalian cell lines and their subclonal derivatives isolated on the basis of increasing resistance to this drug. 8-Azaguanine and 6-thioguanine are synthetic analogs of guanine and are lethal to cells with normal hypoxanthine phosphoribosyltransferase (HPRT) activity. In principle, however, HPRT-positive cells could become selectively resistant to 8-azaguanine if, by any mechanism, the cells expressed higher levels of guanine deaminase. This is because 8-azaguanine, but not 6-thioguanine, is converted by this enzyme to a noncytotoxic metabolite, 8-azaxanthine. Our study shows that HPRT-positive cells inherently resistant to relatively high levels of 8-azaguanine contain high levels of guanine deaminase. In general, guanine deaminase activity was higher in 8-azaguanine-resistant cells, regardless of their HPRT activity. Our results support the view that elevated guanine deaminase activity constitutes a potential mechanism of selective 8-azaguanine resistance in cells with normal HPRT activity. Guanine deaminase levels were significantly elevated in HPRT-positive cells briefly exposed to sublethal concentrations of 8-azaguanine, but this elevation was transient. Long-term exposure of cells to increasingly higher levels of the drug did not lead to high stable levels of guanine deaminase, indicating that 8-azaguanine is not an inducer of guanine deaminase in the cells examined.

ISSN:1424-8581    

DOI:10.1159/000131598

出版商:S. Karger AG    

年代:1981

数据来源: Karger