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. 2016 Apr 25;171(2):1192–1208. doi: 10.1104/pp.15.01976

Figure 1.

Figure 1.

Isolation of mutants that suppress the kanamycin sensitivity of the dms3-4 mutant. A, The phenotype of the wild type (WT), dms3-4, and suppressors of dms3-4 growing on MS medium supplemented with 50 mg/L kanamycin. B, Relative expression of NPTII in the wild type, dms3-4, and suppressors of dms3-4. C, Relative expression of ROS1 in the wild type, dms3-4, and suppressors of dms3-4. D, Relative expression of TSI in wild type, dms3-4, and suppressors of dms3-4. For B, C, and D, RNAs were extracted from 7-d-old seedlings. Values were normalized to the expression level of the references gene (UBI). Two independent experiments (each with three technical replicates) were done with similar results. Values are means ± se, n = 3, from one experiment. E, pold2-1 released the silencing of 35S:NPTII in ros1, ros4, nrpd1, and nrpe1. The growth phenotype of the wild type, pold2-1, ros1, ros4, nrpd1-8, nrpe1-14, and double mutants pold2-1 ros1, pold2-1 ros4, pold2-1 nrpd1-8, and pold2-1 nrpe1-14 on MS containing 0 or 50 mg/L kanamycin (Kan). F, pold2-1 could not restore the expression of silenced RD29A:LUC caused by the ros1 mutant. Luminescence imaging of the RD29A:LUC transgene. The indicated plants were treated with 300 mm NaCl for 3 h followed by luminescence imaging.