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Mutagenesis, Vol. 16, No. 2, 109-114, March 2001
© 2001 UK Environmental Mutagen Society/Oxford University Press

Sequence of centromere separation: effect of 5-azacytidine-induced epigenetic alteration

Maria Jose Rodriguez, Mark A. Lopez1, Africa Garcia-Orad and Baldev K. Vig1,*

Departamento Biologia Animal y Genetica, Facultad de Medicina, Universidad del Pais Vasco/Euskal Herriko Unibertsitatea, Lejona Vizcaya, Spain 48940 and 1 Department of Biology/314, University of Nevada, Reno, NV 89557-0015, USA

The factors which control the sequential separation of the various chromosomes in a genome at the meta-anaphase junction are not well understood. In genomes in which separation is correlated with the quantity of pericentric heterochromatin one factor appears to be the epigenetic nature, namely condensation, of pericentric heterochromatin. When we induced decondensation of pericentric heterochromatin in mouse cells with 10–6, 4x 10–6 and 6x10–6 M 5-azacytidine (5-AC) for 8 h, it resulted in alteration of the sequence of centromere separation. The centromeres which lacked pericentric heterochromatin appeared not to have been affected because there could not be an epigenetic alteration induced by 5-AC. The major effect was on chromosomes with the largest quantity of pericentric heterochromatin. These chromosomes separated at significantly higher frequency than in the untreated population. We also treated human cells, in which separation does not depend upon the quantity of heterochromatin, with 2x10–5 and 6x10–6 M 5-AC for 5 and 8 h. Compared with the control, 5-AC treatment resulted in an increased frequency of separated centromeres of acrocentric chromosomes in relation to those of non-acrocentric chromosomes. In the control the acrocentric chromosomes are the last to separate; in the treated population there was almost random separation of the two types of chromosomes. This epigenetic alteration might be another factor which results in genesis of aneuploidy.

* To whom correspondence should be addressed. Tel: +1 775 784 6544; Fax: +1 775 784 1302; Email: vig{at}med.unr.edu


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