EIN3 interferes with the sulfur deficiency signaling in Arabidopsis thaliana through direct interaction with the SLIM1 transcription factor

- Transcription factor SLIM1 regulating sulfur deficiency response in Arabidopsis binds to DNA as a homodimer.
- SLIM1 can also form heterodimers with EIN3 factor from ethylene signaling pathway and as such is not able to bind to DNA.
- EIN3 negatively impacts the transcription of several SLIM1-dependent genes in sulfur deficiency grown Arabidopsis seedlings.
- The SLIM1 and EIN3 interaction suggests a possible regulatory link between the two pathways.

Sulfur deficiency in plants leads to metabolic reprogramming through changes of gene expression. SLIM1 is so far the only characterized transcription factor associated strictly with sulfur deficiency stress in Arabidopsis thaliana. It belongs to the same protein family as EIN3, a major positive switch of ethylene signaling pathway. It binds to the specific cis sequence called UPE-box. Here we show that SLIM1 interacts with UPE-box as a homodimer. Interestingly, the same region of the protein is used for heterodimerization with EIN3; however, the heterodimer is not able to recognize UPE-box. Expression of several SLIM1-dependent genes is enhanced in sulfur deficiency grown Arabidopsis ein3-1 seedlings (with mutated EIN3 protein). This implies a possible regulatory mechanism of ethylene in sulfur metabolism through direct EIN3-SLIM1 interaction.