SME1 deficiency results in oxidative stress tolerance

In this work, we describe a nonsense mutation in SME1 that alleviates photorespiratory cell death in the Arabidopsis thaliana cat2-2 mutant. A SME1 loss-of-function mutant (sme1-1) and wild-type Col-0 were subjected to mRNA-seq for differential gene expression and alternative splicing analysis. This revealed a massive transcript reprogramming and occurrence of splicing defects caused by SME1 deficiency. For more details see the publication. Overall design: 2 genotypes: sme1-1 and wild-type Col-0 X 3 replicates = 6 samples本研究报道了SME1基因的一处无义突变，该突变可缓解拟南芥（Arabidopsis thaliana）cat2-2突变体中的光呼吸性细胞死亡。我们对SME1功能丧失型突变体（sme1-1）与野生型Col-0开展了mRNA测序（mRNA-seq），以进行差异基因表达与可变剪接分析。结果显示，SME1功能缺失会引发大规模转录组重编程，并导致剪接缺陷的产生。更多细节请参阅相关研究论文。 实验设计概述：2种基因型：sme1-1与野生型Col-0，每种设置3次生物学重复，共计6个样本