Fig. 5: SAGA Gcn5 acetyltransferase activity is linked to protein complex dynamics under DNA replication stress.

a, Fitness assay of the Gcn5 catalytic dead mutant (M) and wild type (WT) strain grown with 100 mM HU. b, Volcano plot showing differential abundance analysis of LiP peptides on HU-induced DNA replication stress in the Gcn5 catalytic dead mutant. Peptide abundances were corrected for protein abundances. P values were calculated by an ANOVA (one-way) and corrected for multiple testing (Benjamini–Hochberg). The dotted horizontal line indicates a significance cutoff of 0.05 for adjusted P values. Blue dots represent FLiP markers of P-body proteins. c, Changes in protein complex network regions identified in the wild type and the Gcn5 catalytic dead mutant on HU stress. The first two columns WT (blue) and M (yellow) indicate the number of changing FLiP markers in the wild type and mutant on HU stress in the respective protein complex. The Δ column is blue if there is a gain in changing FLiP markers in the wild type, yellow if there is a gain in the mutant, gray if there the same markers change in both wild type and mutant and half blue half yellow if different markers change in the wild type and the mutant. The Gcn5 column indicates whether the protein complex network region contains a Gcn5 acetylation target (green) or not (gray)⁸². d, Time-lapse fluorescence microscopy comparing P-body formation in wild type and gcn5-E173A cells before (5 min), during (1 h 55 min) and after (5 h 55 min) 200 mM HU stress. Scale bar, 5 μm. e, Averaged single-cell quantifications of Dcp2-mNG dispersion index in time-lapse microscopy data during replication stress induced by a pulse of HU (shaded gray area). Error bars indicate 95% confidence intervals (n = 440 wild-type cells and n = 640 Gcn5 mutant cells were quantified).