By G. Obe, A.T. Natarajan

Reprint of: Cytogenetic and Genome learn 2004, Vol. 104, No. 1-4 The function of chromosome aberrations in evolution and human health and wellbeing is definitely well-known. This quantity brings jointly papers summarizing our present knowlege of the constitution of interphase nuclei, chromosome constitution, mechanisms of aberration formation and the sensible program of this information in radiobiology, biomonitoring of human populations and melanoma examine. Molecular cytogenetic thoughts reminiscent of fluorescence in situ hybridization utilizing entire chromosome and quarter particular portray DNA probes were effectively used to spot and quantify chromosome aberrations, that is mirrored in numerous papers of this quantity. The mechanisms of chromosome aberration formation by way of sorts of ionizing radiation are thought of intimately. additionally, the real function of telomeres in protecting chromosome integrity and their involvement in genomic instability are mentioned. a last part is devoted to the medical relevance of chromosome aberrations in human hereditary ailments, e.g. Fanconi anemia or ataxia telangiectasia, and in lots of human cancers characterised through particular translocations or deletions. The examine of chromosome aberrations is of serious relevance in scientific genetics and oncology for prognosis and affliction prevention. hence this booklet is suggested examining for cytogeneticists, radiobiologists, oncologists, and post-graduate scholars of genetics and medication.

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In hamster cell lines where global NER is virtually absent, one report shows that CPD repair by TCR in the DHFR gene is limited to the transcribed region of the transcribed strand (Spivak and Hanawalt, 1996). While human cells show efficient global NER, TCR is so rapid that 24 h after UVC irradiation, large regions exist which are CPD free. These CPD-free regions are especially apparent in Xeroderma pigmentosum type C (XPC) fibroblasts (Kantor and Deiss-Tolbert, 1995). , 1990). CPD-free domains do not form in Cockayne syndrome fibroblasts (Shanower and Kantor, 1997), cells that lack TCR activity and retain only global Supported by NIH grant 1PO1CA69449.

Magana-Schwencke N, Henriques JA, Chanet R, Moustacchi E: The fate of 8-methoxypsoralen photoinduced crosslinks in nuclear and mitochondrial yeast DNA: comparison of wild type and repair deficient strains. Proc natl Acad Sci USA 79:1722– 1726 (1982). McHugh PJ, Sones WR, Hartley JA: Repair of intermediate structures produced at DNA interstrand cross-links in Saccharomyces cerevcisiae. Mol Cell Biol 20:3425–3433 (2000). Meetei AR, de Winter JP, Medhurst AL, Wallisch M, Waisfisz Q, van de Vrugt HJ, Oostra AB, Yan Z, Ling C, Bishop CE, Hoatlin ME, Joenje H, Wang W: A novel ubiquitin ligase is deficient in Fanconi anemia.

Cytogenet Genome Res 104:28–34 (2004) Takata M, Sasaki MS, Tachiiri S, Fukushima T, Sonoda E, Schild D, Thompson LH, Takeda S: Chromosome instability and defective recombinational repair in knockout mutants of the five Rad51 paralogs. Mol Cell Biol 21:2858–2866 (2001). Thompson LH, Schild D: The contribution of homologous recombination in preserving genome integrity in mammalian cells. Biochimie 81:87–105 (1999). Tsubouchi H, Ogawa H: A novel mre11 mutation impairs processing of double-strand breaks of DNA during both mitosis and meiosis.

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