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Báo cáo y học: "Chromatin remodeling and genome stability"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Minireview cung cấp cho các bạn kiến thức về ngành y đề tài: Chromatin remodeling and genome stability. | Meeting report Chromatin remodeling and genome stability Gráinne Barkess Address Division of Cancer Sciences and Molecular Pathology University of Glasgow Western Infirmary Glasgow G11 6NT UK. Email g.barkess@clinmed.gla.ac.uk Published 30 June 2006 Genome Biology 2006 7 319 doi l0.ll86 gb-2006-7-6-3l9 The electronic version of this article is the complete one and can be found online at http genomebiology.com 2006 7 6 319 2006 BioMed Central Ltd A report on the 12th Tenovus Scotland Symposium Stability and Regulation of Genes and Genomes Glasgow UK 6-7 April 2006. A feature of many cancer cells is loss of genome stability. They become more prone to mutation and accumulate chromosomal rearrangements. The factors that impinge on genome stability are thus of great interest and a recent meeting in Glasgow sponsored by the cancer charity Tenovus Scotland was an opportunity for researchers in disciplines such as DNA replication repair and recombination and the epigenetic control of gene regulation to learn about the overlapping mechanisms of chromatin remodeling and epigenetics in controlling these diverse functions. Lessons from archaea and yeast With the focus of the meeting mainly on higher eukaryotic cells crossover of information from an unusual model system featured in the Tenovus-Scotland Medal lecture by Stephen Bell MRC Cancer Cell Unit Cambridge UK . Genome stability depends on the faithful replication of DNA and the DNA replication machinery of the unicellular archaea is a helpfully simplified version of that found in eukaryotes. Like eukaryotic chromosomes the DNA of the archaeon Sulfolobus solfataricus contains multiple origins of replication and its primase is a stripped-back version of the eukaryotic DNA polymerase-primase being composed of a small and a large primase subunit only. It appears that histidine residues at the primase active site change conformation to help release the primer and Bell noted that small molecules designed to block this .