Figure 6. H3pT11 affects CLS by regulation of acetic acid resistance.

(A) Relative viability of H3T11A and cka1Δ mutants compared to their WT strains after exposure to indicated durations and concentrations of acetic acid. (B) Acetic acid resistance of WT, sch9Δ, cka1Δ, and sch9Δcka1Δ. (C) CLS assays of WT and H3T11A strains in buffered (pH 6.0) or unbuffered conditions. (D) H3pT11 levels in WT and cka1Δ upon 50 mM acetic acid addition analyzed by western blots (upper). The relative band intensities of H3pT11 to H3 signals (lower). (E) H3pT11 levels in WT, sch9Δ, cka1Δ, and sch9Δcka1Δ at 2 hr after 50 mM acetic acid treatment analyzed by western blots (upper). The relative ratios of H3pT11 to H3 signals (lower). All error bars indicate STD from three biological replicates.

Figure 6—figure supplement 1. H3pT11 regulates CLS by modulation of acid stress response.

(A) Media pH in WT cultures during CLS assay (B) Media acetate concentration in WT cultures at indicated times. (C) CLS assays of WT and cka1Δ strain cultured in SDC media buffered at pH 6.0. (D) Media glucose concentrations of WT strain cultures in SDC media (no acetic acid) or SDC media supplemented with 10 or 50 mM acetic acid. ‘0 hr’ refers to the time at which acetic acid was added. From (A) to (D), All error bars indicate standard deviation (STD) of three biological replicates. (E) H3pT11 levels in WT strain upon treatment of 10 or 50 mM acetic acid measured by Western blots.