Replication forks, chromatin loops and dormant replication origins 英文参考文献.docVIP

Minireview Replication forks, chromatin loops and dormant replication origins J Julian Blow and Xin Quan Ge Address: Wellcome Trust Centre for Gene Regulation and Expression, College of Life Sciences, University of Dundee, Dow Street, Dundee DD1 5EH, UK. Correspondence: J Julian Blow. Email: j.j.blow@dundee.ac.uk Published: 30 December 2008 Genome Biology 2008, 9:244 (doi:10.1186/gb-2008-9-12-244) The electronic version of this article is the complete one and can be found online at /2008/9/12/244 ? 2008 BioMed Central Ltd Abstract When DNA replication is slowed down, normally dormant replication origins are activated. Recent work demonstrates that cells adapt by changing the organization of chromatin loops and maintaining the new pattern of origin use in subsequent cell cycles. It is critical that chromosomal DNA is precisely duplicated during S phase of the eukaryotic cell cycle, with no sections of DNA left unreplicated or replicated more than once. There is a considerable plasticity in this process because cells license many potential replication origins, of which only a small percentage are used in any one cell cycle, with the others remaining ‘dormant’. This means that the usage of replica- tion origins can change under different circumstances. For example, dormant replication origins can be activated when replication forks are inhibited to allow timely completion of the replication programme. A recent paper published in Nature by Courbet et al. [1] illustrates this plasticity of replication origin usage and shows that it is associated with longer-term changes to the organization of chromatin loops. The changes to chromatin organization can then directly affect the way that replication origins are used in subsequent cell cycles. During late mitosis and early G1, the cell licenses replication origins for use in the upcoming S phase by loading protein complexes composed