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. 2024 Sep 5;187(18):5029–5047.e21. doi: 10.1016/j.cell.2024.07.017

Figure 7.

Figure 7

Histone recycling function of Mrc1 is conserved in mammalian cells

(A) (top) Mouse CLASPIN with annotated domains (BP1 and BP2: basic patch 1 and 2, CKBD: Chk1 binding domain, AP: acidic patch) and alignment with Polα and Mcm2 HBDs. (Bottom) overview of mutation in CLASPINΔYY.

(B) WB analysis of WT and CLASPIN mutant mESCs.

(C) Cell-cycle distribution based on mean EdU intensity and total DAPI intensity of WT and CLASPIN mutant mESCs.

(D) High-content microscopy of mean EdU intensity in WT and CLASPIN mutant mESCs.

(E) Average SCAR-seq profile of H3K27me3 and H4K20me0 in WT and CLASPIN mutant mESCs. (C–E) n = 2 biological replicates.

(F) Model: Mrc1 acts as a central coordinator of histone-based inheritance though its ability to bind and transfer H3-H4 tetramers to both leading and lagging strands, with the latter involving joint histone binding with Mcm2 to facilitate transfer to Polα and the lagging strand.