Ghosh M, Liu G, Randall G, Bevington J, Leffak M
Department of Biochemistry and Molecular Biology, Wright State University School of Medicine, 3640 Colonel Glenn Highway, Dayton, OH 45435, USA.
Mol Cell Biol. 2004 Dec;24(23):10193-207. doi: 10.1128/MCB.24.23.10193-10207.2004.
The observation that transcriptionally active genes generally replicate early in S phase and observations of the interaction between transcription factors and replication proteins support the thesis that promoter elements may have a role in DNA replication. To test the relationship between transcription and replication we constructed HeLa cell lines in which inducible green fluorescent protein (GFP)-encoding genes replaced the proximal approximately 820-bp promoter region of the c-myc gene. Without the presence of an inducer, basal expression occurred from the GFP gene in either orientation and origin activity was restored to the mutant c-myc replicator. In contrast, replication initiation was repressed upon induction of transcription. When basal or induced transcription complexes were slowed by the presence of alpha-amanitin, origin activity depended on the orientation of the transcription unit. To test mechanistically whether basal transcription or transcription factor binding was sufficient for replication rescue by the uninduced GFP genes, a GAL4p binding cassette was used to replace all regulatory sequences within approximately 1,400 bp 5' to the c-myc gene. In these cells, expression of a CREB-GAL4 fusion protein restored replication origin activity. These results suggest that transcription factor binding can enhance replication origin activity and that high levels of expression or the persistence of transcription complexes can repress it.
转录活跃基因通常在S期早期进行复制这一观察结果,以及转录因子与复制蛋白之间相互作用的观察结果,支持了启动子元件可能在DNA复制中起作用这一论点。为了测试转录与复制之间的关系,我们构建了HeLa细胞系,其中可诱导的绿色荧光蛋白(GFP)编码基因取代了c-myc基因近端约820 bp的启动子区域。在没有诱导剂的情况下,GFP基因无论以何种方向都会发生基础表达,并且突变型c-myc复制起点的活性得以恢复。相反,转录诱导后复制起始受到抑制。当α-鹅膏蕈碱的存在使基础转录或诱导转录复合物减慢时,复制起点活性取决于转录单元的方向。为了从机制上测试基础转录或转录因子结合是否足以通过未诱导的GFP基因拯救复制,使用GAL4p结合盒取代了c-myc基因5'端约1400 bp内的所有调控序列。在这些细胞中,CREB-GAL4融合蛋白的表达恢复了复制起点活性。这些结果表明,转录因子结合可以增强复制起点活性,而高水平表达或转录复合物的持续存在则可以抑制它。