Fig. 5: The hot5-4 mutant shows the tolerance phenotype of ER stress under Tm treatment. | Nature Communications

Fig. 5: The hot5-4 mutant shows the tolerance phenotype of ER stress under Tm treatment.

From: FAT-switch-based quantitative S-nitrosoproteomics reveals a key role of GSNOR1 in regulating ER functions

Fig. 5: The hot5-4 mutant shows the tolerance phenotype of ER stress under Tm treatment.The alternative text for this image may have been generated using AI.

a Analysis of S-nitrosylation of CNX and CRT proteins in wild type and hot5-4 seedlings by in vivo biotin-switch method. The blots were detected by the anti-CRT and anti-CNX antibody, respectively. Images shown are representative of at least two independent experiments. b Phenotype of wild type (WT) and hot5-4 with or without Tm treatment. Photograph were taken after growing at 22 °C for 9 days. c Fresh weight of WT and hot5-4 plants with or without Tm treatment. Error bars, SD (n = 3 biological represents and each replicate consisting of 10 seedlings). ***p < 0.001, two-tail unpaired t test. d Chlorophyll content of WT and hot5-4 plants with or without Tm treatment. Error bars, SD ((n = 3 biological represents and each replicate consisting of 10 seedlings). *p < 0.05. two-tailed unpaired t test. e–h Expression of BiP3, BiP1,2, ERDJ3A and SHD in wild type (WT) and hot5-4 with or without Tm treatment. Error bars, SD (n = 3 biological replicates). *p < 0.05, **p < 0.01, ***p < 0.001, two-tailed unpaired t test.

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