Biocenter, Botanical Institute, University of Cologne, Germany.
Division of Biological Sciences, Cell and Developmental Biology Section, University of California, La Jolla, CA, USA.
FEBS Lett. 2021 Jun;595(12):1696-1707. doi: 10.1002/1873-3468.14096. Epub 2021 May 19.
The transcriptional regulators of arsenic-induced gene expression remain largely unknown. Sulfur assimilation is tightly linked with arsenic detoxification. Here, we report that mutant alleles in the SLIM1 transcription factor are substantially more sensitive to arsenic than cadmium. Arsenic treatment caused high levels of oxidative stress in the slim1 mutants, and slim1 alleles were impaired in both thiol accumulation and sulfate accumulation. We further found enhanced arsenic accumulation in roots of slim1 mutants. Transcriptome analyses indicate an important role for SLIM1 in arsenic-induced tolerance mechanisms. The present study identifies the SLIM1 transcription factor as an essential component in arsenic tolerance and arsenic-induced gene expression. Our results suggest that the severe arsenic sensitivity of the slim1 mutants is caused by altered redox status.
砷诱导基因表达的转录调控因子在很大程度上仍然未知。硫同化与砷解毒密切相关。在这里,我们报告说,SLIM1 转录因子的突变等位基因对砷比对镉敏感得多。砷处理导致 slim1 突变体中产生高水平的氧化应激,并且 slim1 等位基因在巯基积累和硫酸盐积累方面都受到损害。我们进一步发现 slim1 突变体的根中砷积累增加。转录组分析表明 SLIM1 在砷诱导的耐受机制中起着重要作用。本研究将 SLIM1 转录因子鉴定为砷耐受和砷诱导基因表达的必需组成部分。我们的结果表明,slim1 突变体的严重砷敏感性是由氧化还原状态改变引起的。