TRF2-RAP1 is required to protect telomeres from engaging in homologous recombination-mediated deletions and fusions

Rekha Rai, Yong Chen, Ming Lei and Sandy Chang ()
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Rekha Rai: Yale University School of Medicine
Yong Chen: National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
Ming Lei: National Center for Protein Science Shanghai, State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
Sandy Chang: Yale University School of Medicine

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract Repressor/activator protein 1 (RAP1) is a highly conserved telomere-interacting protein. Yeast Rap1 protects telomeres from non-homologous end joining (NHEJ), plays important roles in telomere length control and is involved in transcriptional gene regulation. However, a role for mammalian RAP1 in telomere end protection remains controversial. Here we present evidence that mammalian RAP1 is essential to protect telomere from homology directed repair (HDR) of telomeres. RAP1 cooperates with the basic domain of TRF2 (TRF2B) to repress PARP1 and SLX4 localization to telomeres. Without RAP1 and TRF2B, PARP1 and SLX4 HR factors promote rapid telomere resection, resulting in catastrophic telomere loss and the generation of telomere-free chromosome fusions in both mouse and human cells. The RAP1 Myb domain is required to repress both telomere loss and formation of telomere-free fusions. Our results highlight the importance of the RAP1-TRF2 heterodimer in protecting telomeres from inappropriate processing by the HDR pathway.

Date: 2016
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DOI: 10.1038/ncomms10881

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