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. 2016 Jun 23;5:e16691. doi: 10.7554/eLife.16691

Figure 7. Salt-induced transcriptional memory leads to dimethylation of H3K4 and binding of poised RNAPII.

Figure 7.

(A) mRNA levels of three genes that exhibit transcriptional memory (PGM2, PMT5 & YGP1) and one gene that does not (HSP31) at the indicated times after treatment with 0.5mM H2O2. Prior to treatment with H2O2, cells were grown either in rich media (no salt; red lines) or treated with 0.7M NaCl for 1 hr and then allowed to recover for 2 hr in rich media (after salt; blue lines). mRNA levels were quantified relative to ACT1 by RT-qPCR. Shown are the averages of three biological replicates ± standard error of the mean. *p<0.05, compared with the same time point in the no salt culture (Student’s t-test). (B) mRNA levels of three genes that exhibit transcriptional memory (PGM2, PMT5 & YGP1) and one gene that does not (HSP31) from set3∆ mutant cells at the indicated times after treatment with 0.5 mM H2O2 same data as in (A). (C and D) ChIP against RNAPII (C), H3K4me2 (D) from wild-type and set3∆ cells grown either in the absence of salt (no salt) or treated with 0.7M NaCl for 1 hr and allowed to recover for 2 hr in rich medium (after salt). (E) ChIP against Ssn3-FRB-GFP cells grown either in the absence of salt (no salt) or treated with 0.7M NaCl for 1 hr and allowed to recover for 2 hr in rich medium (after salt). All ChIP experiments are averages of three biological replicates ± standard error of the mean, quantified as in panel 1A, using primers to amplify the promoters of the indicated genes. *p<0.05, compared with the no salt condition (Student’s t-test).

DOI: http://dx.doi.org/10.7554/eLife.16691.013