大肠杆菌（Escherichia coli）细胞有几种不同DNA修复途径，确保其基因组的稳定性，真核细胞也有相似的DNA修复机制。我们发现功能尚不清楚的基因，ybfE删除或过表达YbfE蛋白都会引起DNA损伤；YbfE蛋白与染色体DNA共定位；ybfEdinI和ybfEdinB双突变体对UV更敏感；复制起始蛋白DnaA影响ybfE基因表达, ybfE启动子含有LexA结合位点。本项目以揭示以上生命现象背后机理为目标，通过遗传学和生物化学与分子生物学手段，阐明由YbfE介导的DNA 修复机制、YbfE与染色体共定位的生物学意义、鉴定YbfE生物学功能；研究DnaA和LexA对ybfE基因表达的协同调控机制。DNA损伤、修复缺陷、DNA异常复制会降低基因组的稳定性，并由此引发细胞癌变或发育缺陷。所以，本项研究不仅在生命科学基础研究中具重要意义，而且在医学研究和临床应用方面也具有借鉴和指导作用。

The Escherichia coli cells have several pathways of DNA repair to maintain the integrity of genome. The eukaryotic cells also have similar mechanisms to repair damaged DNA. We found that deletion of the ybfE gene which is not yet clarified funtionally and overexpression of the YbfE protein led to DNA damage. The YbfE protein was also found to co-localize with the chromosomal DNA. The ybfEdinI and ybfEdinB double mutants were more sensitive to UV relative the single mutants. Interestingly, the replication initiator DnaA affected expression of the ybfE gene and the ybfE promoter region contained a LexA-binding site. However, the mechanisms behind the findings have remained unclear. Here we plan to characterize YbfE-mediated DNA repair pathways using genetic, biochemical and molecular biological methods，to understand why YbfE co-localizes with DNA in vivo and what the fuctions of YbfE are. It has also been designed to investigate interaction of DnaA and LexA, and roles of such interactions in control of ybfE gene expression. DNA damage, repair defeciencies, and uncontrolled replication leads to different diseases including cancers as a result of genome instability. Therefore, the project will shed light on the regulation of DNA repair pathways of both normal and cancer cells.