Figure 3.

Altered basal and acquired thermotolerance of strs1 and strs2 mutants. A, Basal thermotolerance. Stratified seeds sown on MS plates were exposed to 45°C for 3 h and then allowed to germinate and grow at 22°C. A representative plate is shown 6 d after transfer to 22°C. WT, Wild type; hot1-3, a mutant of HSP101 that is defective in basal and acquired thermotolerance (Hong and Vierling, 2000). B, Quantification of basal thermotolerance by percentage of germination of seeds treated at 45°C for 3 h. The results from two independent alleles of strs1 and strs2 are shown. Data are mean ± sd (n = 3). Fisher's protected lsd test showed that all strs mutant lines exhibited a significantly higher germination percentage than wild type and hot1-3 (P ≤ 0.05). C, Quantification of basal thermotolerance by hypocotyl elongation assay using two independent alleles of strs1 and strs2. Seeds were treated at 45°C for the indicated time periods and allowed to germinate in the dark on vertical plates. Hypocotyl length was measured 6 d after transfer to 22°C. Data are mean ± sd (n = 4). Each replicate consisted of approximately 20 seedlings. Bars with different letters indicate significant difference at P ≤ 0.05 (Fisher's protected lsd test). D, Acquired thermotolerance. Seedlings were grown on vertical plates in the dark for 3 d. Con, Control seedlings maintained at 22°C; PT, pretreatment of 38°C for 90 min; HS, heat stress of 45°C for 2 h; PT + 2, pretreatment followed by 2 h at 22°C and then 45°C for 2 h; PT + 3, pretreatment followed by 2 h at 22°C and then 45°C for 3 h. After heat treatment, seedlings were grown for a further 3 d before measurement of the post-stress increase in hypocotyl length. Data are mean ± sd (n = 4). Each replicate consisted of approximately 15 to 20 seedlings. Bars with different letters indicate significant difference at P ≤ 0.05 (Fisher's protected lsd test).