Abstract:
:The Nuclear Pore Complex (NPC) has emerged as an important hub for processing various types of DNA damage. Here, we uncover that fusing a DNA binding domain to the NPC basket protein Nup1 reduces telomere relocalization to nuclear pores early after telomerase inactivation. This Nup1 modification also impairs the relocalization to the NPC of expanded CAG/CTG triplet repeats. Strikingly, telomerase negative cells bypass senescence when expressing this Nup1 modification by maintaining a minimal telomere length compatible with proliferation through rampant unequal exchanges between sister chromatids. We further report that a Nup1 mutant lacking 36 C-terminal residues recapitulates the phenotypes of the Nup1-LexA fusion indicating a direct role of Nup1 in the relocation of stalled forks to NPCs and restriction of error-prone recombination between repeated sequences. Our results reveal a new mode of telomere maintenance that could shed light on how 20% of cancer cells are maintained without telomerase or ALT.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Aguilera P,Whalen J,Minguet C,Churikov D,Freudenreich C,Simon MN,Géli Vdoi
10.1038/s41467-019-13979-5subject
Has Abstractpub_date
2020-01-09 00:00:00pages
160issue
1issn
2041-1723pii
10.1038/s41467-019-13979-5journal_volume
11pub_type
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