Correction to Mengwasser KE, Adeyemi RO, Leng Y et al. Molecular Cell, 2019

Published: 30-07-2020| Version 1 | DOI: 10.17632/h6mrnn4zvb.1
Kristen Mengwasser,
Richard Adeyemi,
Yumei Leng,
Mei Yuk Choi,
Stephen Elledge


In our paper, we reported a striking dependence of BRCA2-deficient cells on the function of the apurinic/apyrimidinic (AP) endonuclease Ape2 (APEX2). Our paper included rescue experiments with various mutants to verify this finding and to clarify the mechanism. In Figures 4I-J, for the gRNA-resistant APEX2 mutant that lacks a functional PIP-box PCNA-binding motif, we inadvertently tested APEX2 R339A instead of APEX2 Y396A/F397A. Consequently, we generated the gRNA-resistant Y396A/F397A APEX2 mutant and tested its ability to rescue the growth defect caused by gRNA-mediated APEX2 depletion, in ovarian BRCA2 mutant cells. In contrast to the result shown in Figures 4I-J, we found that the PIP-box double mutant (Y396A/F397A) does rescue the growth defect caused by gRNA-mediated depletion of APEX2. Thus, we conclude that while the catalytic activity of APEX2 is required for its ability to promote the survival of BRCA2 mutant cells, its PCNA-binding activity is not. We apologize for this error, however it does not affect the overall observation of our paper regarding BRCA2's synthetic lethality with APEX2 loss.


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