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Fig. 1. | Virology Journal

Fig. 1.

From: Strategies to improve homology-based repair outcomes following CRISPR-based gene editing in mosquitoes: lessons in how to keep any repair disruptions local

Fig. 1.

53BP1 influences repair pathway choice. A DSB which has had initial repair factors recruited (MRN complex, ATM, MDC1) and adjacent to a nucleosome with ubiquitylated Lys15 of histone 2A (H2AK15ub) and mono- or di-methylated Lys20 of histone 4 (H4K20me1/2). B In G1 phase, 53BP1 binds to H2A15ub and H4K20me1/2 via its UDR motif and tudor domain respectively. RIF1 is recruited to 53BP1 via binding to ATM-phosphorylated residues. BRCA1 foci formation is inhibited in G1 via 53BP1 and RIF1, where the N terminus ATM target sites in 53BP1 are necessary for its ability to recruit and interact with RIF1 and PTIP. ATM-phosphorylation of 53BP1 leads to recruitment of other NHEJ-promoting factors such as PTIP and EXPAND1, and leads to blocking of end resection and promotion of NHEJ. C In G2/S phases, CtIP is recruited by and bound to the MRN complex. After CtIP is phosphorylated, BRCA1 binds, 53BP1-RIF1 are inhibited from binding to chromatin, and end resection and HDR are promoted. For all panels, colored fill indicates protein factors are conserved in vector mosquiotes, while while fill (CtIP, BRCA1) indicates repairs factors that appear to be absent in mosquitoes

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Virology Journal

ISSN: 1743-422X