http://http://dspace.unitus.it:80 The DSpace digital repository system captures, stores, indexes, preserves, and distributes digital research material. Wed, 22 May 2013 03:53:55 GMT 2013-05-22T03:53:55Z http://hdl.handle.net/2067/1699 Title: Distribution of UVC-induced chromosome aberrations along the X chromosome of TCR deficient and proficient Chinese hamster cell lines. Authors: Martínez-López, Wilner; Marotta, Edvige; Di Tommaso, Maria Valeria; Méndez-Acuña, Leticia; Palitti, Fabrizio Abstract: Cells with a transcription coupled repair (TCR) deficiency are characterized by a higher sensitivity to UVC irradiation and by an increase in apoptosis and chromosomal aberration frequencies. It has been claimed that the higher frequency of chromosomal aberrations results from the transcription blockage caused by UVC-lesions located in the transcribed strands of the genome. The distribution of chromosome breakpoints in euchromatic and heterochromatic regions of the X chromosome from TCR deficient and proficient Chinese hamster cell lines was studied. Most UVC-induced breakpoints occurred in euchromatic regions of the X chromosome in both cell lines. No increase of UVC-induced breakpoints in the euchromatic region of the UV61 X chromosome was observed, indicating that TCR failure alone cannot be responsible for the increased frequency of chromosomal aberrations. Differential chromatin remodeling in the TCR defective cell line is proposed as a possible mechanism involved in the distribution of UVC-induced breakpoints along the Chinese hamster X chromosome. A similar explanation for the increase of UVC-induced chromosomal aberrations in TCR defective cells is given Description: L'articolo è disponibile sul sito dell'editore: http://www.sciencedirect.com Thu, 31 Dec 2009 23:00:00 GMT http://hdl.handle.net/2067/1699 2009-12-31T23:00:00Z http://hdl.handle.net/2067/1702 Title: Histone post-translational modifications in DNA damage response Authors: Méndez-Acuña, Leticia; Di Tommaso, Maria Valeria; Palitti, Fabrizio; Martínez-López, Wilner Abstract: The fact that eukaryotic DNA is packed into chromatin constitutes a physical barrier to enzymes and regulatory factors to reach the DNA molecule for replication, transcription, recombination and repair. Although most studies in this field have concentrated on how chromatin regulates transcription, there is a recent emphasis on studying the role of chromatin in the response to DNA damage. Two main chromatin-remodeling mechanisms have been identified, namely, ATP-dependent chromatin-remodeling complexes and histone post-translational modifications (PTMs). PTMs constitute reversible covalent modifications in aminoacidic residues, such as serine and threonine phosphorylation, lysine acetylation, lysine and arginine methylation and lysine ubiquitylation, among others. Moreover, nucleosome composition can be modified by the incorporation of histone variants, which are assembled into nucleosomes independently of DNA replication. The phosphorylation of the histone variant H2AX (gammaH2AX) is one of the best examples of histone PTMs in response to DNA damage induction, but many others have recently been revealed. In this review, we focus on and summarize the best-known histone PTMs observed in excision repair (base excision and nucleotide excision) and double-strand break (non-homologous end-joining and homologous recombination) repair pathways. In brief, the interplay between chromatin remodelers and DNA repair factors is discussed in relation to DNA damage response mechanisms. Copyright 2010 S. Karger AG, Basel. PMID: 20407219 Description: L'articolo è diponibile sul sito dell'editore: http://www.karger.com Thu, 31 Dec 2009 23:00:00 GMT http://hdl.handle.net/2067/1702 2009-12-31T23:00:00Z http://hdl.handle.net/2067/1684 Title: Asynchronously Replicating Eu/Heterochromatic Regions Shape Chromosome Damage. Authors: Di Tommaso, Maria Valeria; Martínez-López, Wilner; Palitti, Fabrizio Abstract: In order to shed more light on the influence of DNA replication on the formation and distribution of chromosome aberrations, breakpoints (BP) produced by UV-C and AluI were assigned either to the early replicating short euchromatic arm (Xpe) or to the late replicating long heterochromatic arm (Xqh) of the Chinese hamster (CHO9) X chromosome. Early (ES) or late (LS) S-phase cells were assessed by pulse incorporating the base analogue 5-bromo-2′-deoxyuridine (BrdU) immediately after UV-C irradiation (30 J/m2) or AluI (20 U) poration followed by BrdU immunodetection with FITC-tagged antibodies in metaphase spreads. Short (30 s) UV-C exposures (1 J/m2/s) induced BP preferentially in Xqh in LS cells and a random distribution of BP along Xpe and Xqh in ES cells. However, BP induced by long (5 min) UV-C exposures (0.1 J/m2/s) clustered according to arm replication time (Xpe during ES and Xqh along LS). Giemsa-stained metaphases showed elevated frequencies of UV-C induced chromatid-type aberrations and gaps, especially in cells exposed to longer UV-C irradiation. BP induced by AluI clustered in Xpe in ES but distributed randomly during LS. In contrast to UV-C, AluI did not produce an increase in the yield of gaps, neither in ES nor in LS cells. Putative mechanisms underlying the observed distributions of chromosome damage in replicating CHO9 cells exposed to UV-C and AluI are discussed. Description: L'articolo è disponibile sul sito dell'editore: http://www.karger.com. Thu, 31 Dec 2009 23:00:00 GMT http://hdl.handle.net/2067/1684 2009-12-31T23:00:00Z http://hdl.handle.net/2067/1695 Title: Relationship between DNA Repair and Formation of Sister Chromatid Exchanges and Chromatid Aberrations under the Influence of Poly(ADP-Ribose) Polymerase Inhibition by 3-Aminobenzamide Authors: Filippi, Silvia; Palitti, Fabrizio; Martínez-López, Wilner; Natarajan, Adayapalam T. Abstract: The mechanisms of formation of sister chromatid exchanges (SCEs) and chromosome aberrations following inhibition of poly(ADP-ribose) polymerase by 3-aminobenzamide were studied in Chinese hamster ovary cell lines deficient in different repair pathways. The results confirm earlier findings that (a) the 'spontaneous' SCEs are formed due to the incorporated BrdU in the DNA, (b) 'spontaneous' and induced SCEs originate from different mechanisms, and (c) SCEs and chromatid exchanges are formed by different pathways. Description: L'articolo é disponibile sul sito dell'editore: http://www.karger.com Thu, 31 Dec 2009 23:00:00 GMT http://hdl.handle.net/2067/1695 2009-12-31T23:00:00Z