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. 2013 Dec 27;111(2):699–704. doi: 10.1073/pnas.1316433111

Fig. 5.

Fig. 5.

Functional analysis of H2B-K123 in H2B-H2A and H2B-Htz1 fusions. (A) Schematic representation of nucleosomes containing nonfused or fused H2B-K123A point mutants. The cell strains examined were as follows: (1) nonfused WT H2B; (2) nonfused H2B(K123A); (3) fused H2B-H2A/H2B-Htz1; (4) fused H2B(K123A)-H2A/H2B(K123A)-Htz1; (5) fused H2B(K123A)-H2A/H2B(WT)-Htz1; and (6) fused H2B(WT)-H2A/H2B(K123A)-Htz1. (B) Drug sensitivity analysis of fused H2B-H2A and/or H2B-Htz1 with the H2B-K123A point mutation. (C) Immunoblot analysis of monoubiquitination of H2B-K123 in H2B-H2A and H2B-Htz1. Lanes labeled 1 show a series of fourfold dilutions of samples from WT cells. Histone H4 was used as a loading control.