Fig. 5.

The synthetic thermotolerance of the Spt16-depleted strain is determined by the defect of nucleosome assembly at heat shock gene promoters during sustained stress, leading to increased expression of molecular chaperones. a ChIPs using anti-SPT16 antibody were performed for the tet-SPT16 cell culture grown at 30 °C or heat shocked at 37 °C for 16 min, and data for the HSP12, HSP82, and SSA4 promoters are shown. For each panel, Y-axis: abundance of SPT16 relative to the chromosome V intergenic region. X-axis: data for 30 °C and for 37 °C shown. b ChIPs using an anti-histone H3 antibody were performed for the tet-SPT16 cell culture consistently grown at 37 °C in the absence (−Dox) or presence (+Dox) of doxycycline. For each panel, Y-axis: abundance of histone H3 (inverse ration of histone loss) relative to chromosome V intergenic region. X-axis: data shown for cultures consistently grown at 37 °C in the absence (−Dox) or presence (+Dox) of doxycycline. c ChIPs using an anti-HSF antibody were performed for the tet-SPT16 cell culture consistently grown at 37 °C in the absence (−Dox) or presence (+Dox) of doxycycline. For each panel: Y-axis: abundance of HSF relative to the chromosome V intergenic region. X-axis: as in b. d ChIPs using an anti-Pol II antibody were performed for the tet-SPT16 cell culture consistently grown at 37 °C in the absence (−Dox) or presence (+Dox) of doxycycline. For each panel: Y-axis: abundance of Pol II relative to the chromosome V intergenic region. X-axis: as in b. For all sections of the figure (a, b, c, and d), values represent mean ± S.D. (n ≥ 3). The p values calculated using Student’s t test assuming equal variance are shown in the corner of each subpanel