The study provides new data on the stability of gamma radiation-induced chromosome fragments of a putative maternal nuclear genome in an androgenetic vertebrate, rainbow trout (Oncorhynchus mykiss

Centromeres and telomeres assure stability of eukaryotic chromosomes that undergo multiple segregations during cell divisions (Blackburn and Szostak, 1984). Chromosome movement during mitosis and meiosis is regulated by a centromere, which exists in each chromosome. The protein complex assembled at each centromere, named the kinetochore, serves as an attachment site for spindle microtubules (Cleveland et al., 2003). Centromeres are heterochromatic in most organisms and the role of centromeric heterochromatin has been investigated in regard to sisterchromatid cohesion at metaphase (Bernard and Allshire, 2002). Heterochromatic pericentromeric regions are recognized by conventional cytogenetic techniques such as C-banding or restriction enzyme digestion. Centromeric regions of chromosomes in some teleosts consist of AT-rich chromatin that can be revealed by DAPI banding (Ocalewicz et al., 2003). Ends of eukaryotic chromosomes are capped with nucleoprotein complexes named telomeres, which serve many functions, such as protecting chromosome ends from degradation during the cell cycle and preventing chromosome end-to-end fusions. The DNA component of a telomere is built of short, tandemly repeated G-rich sequences, such as TTAGGG in vertebrates (Blackburn, 2001). Telomeric probes are widely used to investigate chromosomal rearrangements because in many vertebrates they appear frequently at interstitial sites of chromosomes (Meyne et al., 1990). These interstitial telomeric sites (ITS) can be remnants of chromosome rearrangements (fusions or inversions) occurring in genome evolution (Go et al., 2000; Castiglia et al., 2002; Slijepcevic, 1998) or aberrations (Natarajan et al., 1996; Slijepcevic et al., 1997). Telomeres allow the repairing system to distinguish between natural chromosome ends and chromosomal breaks such as double strand breaks (DSB). These can occur spontaneously during DNA replication, formation of dicentric chromosomes followed by breakage during chromosome segregation or by recombination. Also, DSB can be induced experimentally by subjecting DNA to damaging agents, such as radiation, alkylating agents, certain antibiotics or endonucleases (Obe et al., 2002). The naked ends of chromosomes arrest the cell cycle, and the repairing process starts before chromosome aberrations become irreparable and kill the cell (Crompton, 1997). Cellular repairing mechanisms can fix the breaks de novo by healing the chromosome end with a new telomere built by a The Journal of Experimental Biology 207, 2229-2236 Published by The Company of Biologists 2004 doi:10.1242/jeb.01007