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. 2018 Sep 25;9:3925. doi: 10.1038/s41467-018-06407-7

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 5 — FAM35A and C20ORF196 block resection in the BRCA1-deficient cells. a, b The absence of FAM35A (a) or C20ORF196 (b) suppressed the olaparib sensitivity of the BRCA1-deficient cells. The mean and s.d. from three independent experiments are shown. c Chromosome aberration of various DT40 cells. Cells were treated with or without 1 μM olaparib for 8 h and then incubated with 100 ng ml^–1 colcemid for 4 h before fixing. The mean and s.e.m. are shown. d, e Immunofluorescence (d) and its quantification (e) showing that FAM35A and C20ORF196 block the end resection in the BRCA1-deficient cells. The DT40 cells were treated with 4 Gy X-ray and released 4 h before fixing. The mean and s.d. from three independent experiments are shown. Scale, 2 μm. f A scatter diagram shows RAD51 foci numbers in DT40 cells after X-ray treatment. The mean and s.d. are shown. g A model shows that REV7–FAM35A–C20ORF196 complex blocks resection through binding the 5ʹ-recessed DSB ends. *p < 0.05; **p < 0.01; ***p < 0.001; ****p < 0.0001. Statistics was performed by two-tailed t-test