Institute for Plant Sciences, Cluster of Excellence on Plant Sciences, University of Cologne, 50674 Cologne, Germany.
Max Planck Institute of Molecular Plant Physiology, 14476 Potsdam-Golm, Germany.
Plant Physiol. 2020 Dec;184(4):2120-2136. doi: 10.1104/pp.20.01192. Epub 2020 Oct 15.
Sulfur, an indispensable constituent of many cellular components, is a growth-limiting macronutrient for plants. Thus, to successfully adapt to changing sulfur availability and environmental stress, a sulfur-deficiency response helps plants to cope with the limited supply. On the transcriptional level, this response is controlled by SULFUR LIMITATION1 (SLIM1), a member of the ETHYLENE-INSENSITIVE3-LIKE (EIL) transcription factor family. In this study, we identified EIL1 as a second transcriptional activator regulating the sulfur-deficiency response, subordinate to SLIM1/EIL3. Our comprehensive RNA sequencing analysis in Arabidopsis () allowed us to obtain a complete picture of the sulfur-deficiency response and quantify the contributions of these two transcription factors. We confirmed the key role of SLIM1/EIL3 in controlling the response, particularly in the roots, but showed that in leaves more than 50% of the response is independent of SLIM1/EIL3 and EIL1. RNA sequencing showed an additive contribution of EIL1 to the regulation of the sulfur-deficiency response but also identified genes specifically regulated through EIL1. SLIM1/EIL3 seems to have further functions (e.g. in the regulation of genes responsive to hypoxia or mediating defense at both low and normal sulfur supply). These results contribute to the dissection of mechanisms of the sulfur-deficiency response and provide additional possibilities to improve adaptation to sulfur-deficiency conditions.
硫是许多细胞成分中不可或缺的组成部分,是植物生长的限制型大量营养素。因此,为了成功适应不断变化的硫供应和环境胁迫,硫缺乏响应有助于植物应对有限的供应。在转录水平上,这种响应受硫限制 1(SLIM1)的控制,它是乙烯不敏感 3 样(EIL)转录因子家族的一员。在这项研究中,我们确定了 EIL1 作为调节硫缺乏响应的第二个转录激活剂,从属于 SLIM1/EIL3。我们在拟南芥()中的综合 RNA 测序分析使我们能够获得硫缺乏响应的完整图像,并量化这两个转录因子的贡献。我们证实了 SLIM1/EIL3 在控制响应中的关键作用,特别是在根部,但表明在叶片中,超过 50%的响应独立于 SLIM1/EIL3 和 EIL1。RNA 测序表明 EIL1 对硫缺乏响应的调节有附加贡献,但也鉴定了通过 EIL1 特异性调节的基因。SLIM1/EIL3 似乎具有进一步的功能(例如,在调节对缺氧有反应的基因或在低硫和正常硫供应下介导防御方面)。这些结果有助于解析硫缺乏响应的机制,并为改善对硫缺乏条件的适应提供了额外的可能性。