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 (Arabidopsis thaliana) 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成分，是植物生长受限的大量营养素。因此，为了成功适应不断变化的硫供应和环境压力，硫缺乏反应可帮助工厂应对有限的供应。在转录水平上，此反应受EIL转录因子家族成员SLIM1的控制。在这项研究中，我们确定EIL1是第二个转录激活因子，它调节着硫缺乏反应，从属于SLIM1 / EIL3。我们在拟南芥中进行的全面RNA-Seq分析使我们能够完整了解硫缺乏反应并量化这两个转录因子的作用。我们确认了SLIM1 / EIL3在控制响应（尤其是在根部）中的关键作用，但显示在叶片中，超过50％的响应独立于SLIM1 / EIL3和EIL1。RNA-seq显示EIL1对硫缺乏反应的调节具有累加作用，但也鉴定了通过EIL1特异性调节的基因。SLIM1 / EIL3似乎还有其他功能，例如，在低硫和正常硫供应下调节对缺氧或介导防御的基因。这些结果有助于剖析硫缺乏反应的机制，并为改善对硫缺乏条件的适应性提供了其他可能性。SLIM1 / EIL3似乎还有其他功能，例如，在低硫和正常硫供应下调节对缺氧或介导防御的基因。这些结果有助于剖析硫缺乏反应的机制，并为改善对硫缺乏条件的适应性提供了其他可能性。SLIM1 / EIL3似乎还有其他功能，例如，在低硫和正常硫供应下调节对缺氧或介导防御的基因。这些结果有助于剖析硫缺乏反应的机制，并为改善对硫缺乏条件的适应性提供了其他可能性。