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. 2021 Jan 21;49(4):2027–2043. doi: 10.1093/nar/gkab003

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© The Author(s) 2021. Published by Oxford University Press on behalf of Nucleic Acids Research.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 5. — Accumulation of DNA damage in prpf31 mutant retinas. (A) Immunofluorescence analysis using the anti-γH2AX antibody in siblings and prpf31⁻^/⁻ retinas at 36, 48, and 60 hpf. Scale bar, 50 μm. (B) Quantitative analysis of the γH2AX positive cells shown in (A). (C) Alkaline comet assay showed increased DNA damage in prpf31⁻^/⁻ zebrafish at 36 and 48 hpf. Scale bar, 10 μm. White arrows showed DNA with single or double strand breaks. (D) Quantitative results of 100 cells from 6 embryos in each group are shown. White arrows indicate DNA damaged cells. (E) The protein levels of Prpf31, γH2AX and p53 in siblings and prpf31⁻^/⁻ zebrafish at 36, 48 and 60 hpf were detected by western blot. GAPDH was used to normalize protein loading. The black arrows indicated the corresponding protein bands.