cells with low Heat Shock Protein 12 (HSP12) 99%: cells with high HSP12 25% %
||Budding yeast Saccharomyces cerevisiae
||Gilad Yaakov, David Lerner, Kajetan Bentele, Joseph Steinberger and Naama Barkai, Coupling phenotypic persistence to DNA damage increases genetic diversity in severe stress, Nature Ecology & Evolution 1, Article number: 0016 (2017) pdf link doi:10.1038/s41559-016-0016 p.4 left column
||Abstract: "[Investigators] report that spontaneous DNA damage triggers persistence in Saccharomyces cerevisiae
by activating the general stress response, providing protection against a range of harsh stress and drug environments."
||P.2 right column bottom paragraph to p.4 right column: "Consistent with the idea that DNA damage triggers persistence, [investigators] find an increased fraction of persisters in strains showing elevated mutation rates, as indicated by higher fractions of extreme Hsp12-expressing cells with increased stress survival (Supplementary Fig. 4). To verify directly that DNA damage triggers persistence, [they] induced DSBs [double-strand breaks] by expressing a GAL1-inducible HO (homothallic switching) endonuclease in cells with a single HO cleavage site. Inducing HO led to the appearance of Rad52-GFP foci, followed by a delayed (~2 h) induction of Hsp12-mCherry (Fig. 2f,g and Supplementary Fig. 5). Subjecting cells to fluphenazine confirmed that cells became persisters (Fig. 2h and Supplementary Videos 5 and 6). While ~99% of cells with low Hsp12 died within 60 min of exposure, only 25% of high Hsp12 cells died at that time, with survivors losing viability at a significantly lower rate (Fig. 2i). Nearly all survivors had Rad52 foci (Fig. 2h). [They] conclude that a severe DNA damage, such as DSB, triggers persistence in budding yeast."