Replication stress (RS) is intrinsic to normal cell growth, is enhanced by exogenous factors and elevated in many cancer cells due to oncogene expression. Most genetic changes are a result of RS and the mechanisms by which cells tolerate RS has received considerable attention because of the link to cancer evolution and opportunities for cancer cell-specific therapeutic intervention. Site-specific replication fork barriers have provided unique insights into how cells respond to RS and their recent use has allowed a deeper understanding of the mechanistic and spatial mechanism that restart arrested forks and how these correlate with RS-dependent mutagenesis. Here we review recent data from site-specific fork arrest systems used in yeast and highlight their strengths and limitations.

复制应激 (RS) 是正常细胞生长所固有的，由外源因素增强，并且由于癌基因表达而在许多癌细胞中升高。大多数遗传变化是 RS 的结果，细胞耐受 RS 的机制已受到相当多的关注，因为它与癌症进化和癌细胞特异性治疗干预的机会有关。位点特异性复制叉屏障为细胞如何响应 RS 提供了独特的见解，它们最近的使用使我们能够更深入地了解重新启动停滞叉的机制和空间机制，以及这些与 RS 依赖性诱变的关系。在这里，我们回顾了酵母中使用的特定地点叉形制动系统的最新数据，并强调了它们的优势和局限性。