PMID:29227966

Citation	Yu, Y, Tan, R, Ren, Q, Gao, B, Sheng, Z, Zhang, J, Zheng, X, Jiang, Y, Lan, L and Mao, Z (2017) POT1 inhibits the efficiency but promotes the fidelity of nonhomologous end joining at non-telomeric DNA regions. Aging (Albany NY) 9:2529-2543
Abstract	Robust DNA double strand break (DSB) repair and stabilized telomeres help maintain genome integrity, preventing the onset of aging or tumorigenesis. POT1 is one of the six factors in the shelterin complex, which protects telomeres from being recognized as DNA damages. TRF1 and TRF2, two other shelterin proteins, have been shown to participate in DNA DSB repair at non-telomeric regions, but whether POT1, which binds to single strand telomeric DNA at chromosomal ends, is involved in DNA DSB repair has not been assessed. Here we found that POT1 arrives at DNA damage sites upon the occurrence of DNA DSBs. It suppresses the efficiency of nonhomologous end joining (NHEJ), the major pathway for fixing DNA DSBs in mammals, but surprisingly promotes NHEJ fidelity. Mechanistic studies indicate that POT1 facilitates the recruitment of Artemis, which is a nuclease and promotes fidelity of NHEJ, to DNA damage sites. In addition, we found that overexpression of POT1 inhibits the protein stability of Lig3, which is the major regulator of alternative NHEJ (alt-NHEJ), therefore suppressing the efficiency of alt-NHEJ. Taken together we propose that POT1 is a key factor regulating the balance between the efficiency and fidelity of NHEJ at non-telomeric DNA regions.
Links	PubMed PMC5764391 Online version:10.18632/aging.101339
Keywords
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Annotations

Gene product	Qualifier	GO Term	Evidence Code	with/from	Aspect	Extension	Notes	Status
HUMAN:POTE1		GO:2001032: regulation of double-strand break repair via nonhomologous end joining	ECO:0000314:		P		Figure 2 POT1 promotes NHEJ fidelity but inhibits NHEJ efficiency	complete CACAO 13287

References

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