Erratum

BRCA1 and CtIP promote alternative nonhomologous end-joining at uncapped telomeres Sophie Badie, Ana Rita Carlos, Cecilia Folio, Keiji Okamoto, Peter Bouwman, Jos Jonkers & Madalena Tarsounas Correction to: The EMBO Journal (2015) 34: 410–424. DOI 10.15252/embj.201488947 | Published online 12 January 2015

Due to a technical error in the printing process, the colors of figure 7 are displayed incorrectly in the printed issue; the online

version is unaffected by this error. Please find below the correct figure:

shelterin 3’

- TRF2 (partial uncapping) 3’

MRN 3’

ATM

C-NHEJ

A-NHEJ

BRCA1

KU70/80 CtIP MRN

Limited resection 3’

LIG4 TTAGGGTTAGGG

3’

3’

GGGATTGGGATT

3’ 3’

EXO1

LIG3 Figure 7. Model for the role of BRCA1-CtIP in A-NHEJ. Telomeres uncapped by TRF2 depletion undergo 30 overhang excision in MRN-dependent manner. Most telomeres are bound by Ku heterodimer and re-joined by C-NHEJ promoted by 53BP1. A subset of the telomeres become substrates for resection reactions, which require MRN, BRCA1 and CtIP. Initiation of resection generates short 30 telomeric overhangs, whose annealing is facilitated by the homology provided by 2 A-T base pairs per telomeric repeat. The resulting flaps are cleaved by EXO1 and telomeres re-joined through the LIG3-dependent A-NHEJ pathway.

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The EMBO Journal Vol 34 | No 6 | 2015

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BRCA1 and CtIP promote alternative non-homologous end-joining at uncapped telomeres.

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