S Modino1, P Slijepcevic. 1. Brunel Institute of Cancer Genetics and Pharmacogenomics, Brunel University, Uxbridge, UK.
Abstract
PURPOSE: To compare telomere length in mouse strains with constitutional chromosomal aberrations generated either by exposure of parents to ionizing radiation, a chemical mutagen or arising spontaneously with that of the karyotypically normal mouse from the same genetic background. MATERIALS AND METHODS: Telomere length was assessed in five independently derived strains of mouse with constitutional chromosomal aberrations and in the karyotypically normal control mouse using quantitative fluorescence in situ hybridization (Q-FISH). Bone marrow cells obtained directly from the animals were used for the analysis. RESULTS: Chromosomal aberrations, one in each mouse strain, included three reciprocal translocations induced by ionizing radiation, one insertion induced by a chemical mutagen and one spontaneous Robertsonian translocation. There was no cytogenetically detectable loss of material in any of the strains and most mice were phenotypically normal. Telomeres were significantly shorter in all mouse strains with constitutional chromosomal aberrations in comparison with those originating from the karyatypically normal mouse from the same genetic background. Telomeres were significantly shorter at p-arms than at q-arms in all animals. The telomere length in individual chromosomes was variable and there was no single chromosome with consistently short telomeres in all animals. CONCLUSIONS: The presence of stable chromosomal aberrations, such as translocations or insertions, in the mouse genome may generate telomere shortening. This might have implications for understanding biological consequences or radiation-induced stable chromosomal aberrations.
PURPOSE: To compare telomere length in mouse strains with constitutional chromosomal aberrations generated either by exposure of parents to ionizing radiation, a chemical mutagen or arising spontaneously with that of the karyotypically normal mouse from the same genetic background. MATERIALS AND METHODS: Telomere length was assessed in five independently derived strains of mouse with constitutional chromosomal aberrations and in the karyotypically normal control mouse using quantitative fluorescence in situ hybridization (Q-FISH). Bone marrow cells obtained directly from the animals were used for the analysis. RESULTS: Chromosomal aberrations, one in each mouse strain, included three reciprocal translocations induced by ionizing radiation, one insertion induced by a chemical mutagen and one spontaneous Robertsonian translocation. There was no cytogenetically detectable loss of material in any of the strains and most mice were phenotypically normal. Telomeres were significantly shorter in all mouse strains with constitutional chromosomal aberrations in comparison with those originating from the karyatypically normal mouse from the same genetic background. Telomeres were significantly shorter at p-arms than at q-arms in all animals. The telomere length in individual chromosomes was variable and there was no single chromosome with consistently short telomeres in all animals. CONCLUSIONS: The presence of stable chromosomal aberrations, such as translocations or insertions, in the mouse genome may generate telomere shortening. This might have implications for understanding biological consequences or radiation-induced stable chromosomal aberrations.