AI Article Synopsis
- XRCC4-like factor (XLF), also known as Cernunnos, plays a crucial role in the repair of DNA double-strand breaks (DSBs) through the non-homologous end-joining (NHEJ) pathway in mammalian cells.
- XLF enhances DSB repair by facilitating the joining process mediated by XRCC4-ligase IV and is quickly recruited to DSB sites, primarily influenced by the presence of Ku proteins.
- Although XRCC4 is not essential for XLF recruitment, it helps stabilize XLF's binding to DSBs, highlighting XLF's direct involvement in the assembly of the NHEJ repair machinery.
Article Abstract
XRCC4-like factor (XLF)--also known as Cernunnos--has recently been shown to be involved in non-homologous end-joining (NHEJ), which is the main pathway for the repair of DNA double-strand breaks (DSBs) in mammalian cells. XLF is likely to enhance NHEJ by stimulating XRCC4-ligase IV-mediated joining of DSBs. Here, we report mechanistic details of XLF recruitment to DSBs. Live cell imaging combined with laser micro-irradiation showed that XLF is an early responder to DSBs and that Ku is essential for XLF recruitment to DSBs. Biochemical analysis showed that Ku-XLF interaction occurs on DNA and that Ku stimulates XLF binding to DNA. Unexpectedly, XRCC4 is dispensable for XLF recruitment to DSBs, although photobleaching analysis showed that XRCC4 stabilizes the binding of XLF to DSBs. Our observations showed the direct involvement of XLF in the dynamic assembly of the NHEJ machinery and provide mechanistic insights into DSB recognition.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2246615 | PMC |
| http://dx.doi.org/10.1038/sj.embor.7401137 | DOI Listing |
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