加州大學(xué)醫(yī)學(xué)院分子醫(yī)學(xué)和癌癥研究中心,，Ludwig癌癥研究所的科學(xué)家在基因組穩(wěn)定性的研究上去的新的進(jìn)展,，研究性文章Specific pathways prevent duplication-mediated genome rearrangements已發(fā)表在最新一期的Nature上。
萬事萬物都處于運(yùn)動(dòng)當(dāng)中,，細(xì)胞中的基因組也不例外,，基因組可能發(fā)生突變，可能發(fā)生序列重復(fù),，種種的變故導(dǎo)致基因組重排和不穩(wěn)定,。一旦，這些細(xì)微的變化蓄積的多了,，或是在某些關(guān)鍵的部分發(fā)生決定性的變化可能導(dǎo)致機(jī)體機(jī)能發(fā)生變化,，導(dǎo)致疾病甚至癌癥的發(fā)生。
在每個(gè)細(xì)胞中,，有大量的不同的蛋白保護(hù)著基因組,，維持基因組的穩(wěn)定性，防止重排或是錯(cuò)配的發(fā)生,。但是,，究竟是哪些蛋白，哪些基因在這過程中發(fā)揮了重要的作用，科學(xué)家們并不清楚,。
加州大學(xué)的科學(xué)家們研究發(fā)現(xiàn),，在釀酒酵母染色體V左臂中，有13個(gè)基因發(fā)揮著防止基因組重排的作用,。它們分別是:SGS1,TOP3,RMI1,SRS2,RAD6,SLX1,SLX4,SLX5,MSH2,MSH6,RAD10和與DNA復(fù)制監(jiān)測(cè)點(diǎn)有關(guān)的MRC1,、TOF1。
這些研究結(jié)果表明,，真核細(xì)胞有多個(gè)基因保護(hù)基因組穩(wěn)定性,，也為基因組穩(wěn)定性的研究提供了新的思路。（生物谷Bioon.com）
生物谷推薦原始出處：
Nature advance online publication 29 July 2009 | doi:10.1038/nature08217
Specific pathways prevent duplication-mediated genome rearrangements
Christopher D. Putnam1, Tikvah K. Hayes1 & Richard D. Kolodner1
Ludwig Institute for Cancer Research, Departments of Medicine and Cellular and Molecular Medicine and Cancer Center, University of California School of Medicine, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0669, USA
We have investigated the ability of different regions of the left arm of Saccharomyces cerevisiae chromosome V to participate in the formation of gross chromosomal rearrangements (GCRs). We found that the 4.2-kilobase HXT13-DSF1 region sharing divergent homology with chromosomes IV, X and XIV, similar to mammalian segmental duplications, was 'at risk' for participating in duplication-mediated GCRs generated by homologous recombination. Numerous genes and pathways, including SGS1, TOP3, RMI1, SRS2, RAD6, SLX1, SLX4, SLX5, MSH2, MSH6, RAD10 and the DNA replication stress checkpoint requiring MRC1 and TOF1, were highly specific for suppressing these GCRs compared to GCRs mediated by single-copy sequences. These results indicate that the mechanisms for formation and suppression of rearrangements occurring in regions containing at-risk sequences differ from those occurring in regions of single-copy sequence. This explains how extensive genome instability is prevented in eukaryotic cells whose genomes contain numerous divergent repeated sequences.
