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| Ethylene signaling: MAPKing new pathways
Two antagonistic MAPK pathways regulate ethylene signaling in plants through differential phosphorylation of the transcription factor EIN3. The plant hormone ethylene mediates development, differentiation and stress signaling in Arabidopsis thaliana by regulating MAP kinase (MAPK) cascades. In the absence of ethylene, the Raf-like MAPKKK CTR1 (constitutive triple response 1) represses signaling by directly interacting with the ethylene receptor ETR1. Ethylene inhibits CTR1 activity to relieve this repression, resulting in the activation of an unknown MAPK module that promotes EIN3 (ethylene-insensitive 3) transcriptional activity. In Nature, Yoo et al. now uncover the identity of this MAPK module by showing that ethylene activates the MKK9–MPK3/6 MAPK pathway, and describe how ethylene signaling is regulated through differential phosphorylation of EIN3.
The authors performed a genetic screen in CTR1-deficient cells to identify novel MAPK components of the ethylene response pathway. The screen uncovered the kinase MKK9, which directly phosphorylated and activated MPK3/6 in vitro. The ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC) upregulated MPK3/6 in wild-type, but not MKK9-deficient leaves. Furthermore, constitutively active MKK9 induced a phenotype consistent with continuous exposure to ethylene, suggesting that MKK9–MPK3/6 is a critical positive regulator of ethylene signaling. Transgenic epistasis analysis placed MKK9 downstream of ETR1 and upstream of EIN3 in the ethylene signaling pathway. Furthermore, MPK3/6 directly phosphorylated EIN3 at Thr 174 in vitro. Phosphorylation at this residue in vivo stabilized EIN3 and promoted its nuclear accumulation; in addition, constitutively active MKK9 robustly induced EIN3-responsive genes. Therefore, the MKK9–MPK3/6 axis promotes the response to ethylene by phosphorylating EIN3 at Thr 174, which upregulates its nuclear accumulation and transcriptional activity. How does CTR1 negatively regulate the ethylene pathway? Constitutively active CTR1 reduced EIN3 protein levels, but had no effect on EIN3 with a mutation at the Thr 592 position. As Thr 592 is a consensus MAPK phosphorylation site, the authors speculate that CTR1 induces phosphorylation at this site, thereby mediating EIN3 degradation. The kinase responsible for phosphorylating Thr 592 in vivo has not yet been identified. These data suggest that ethylene–ETR1 signaling activates MKK9, which phosphorylates MPK3/6. Active MPK3/6 then phosphorylates EIN3 at Thr 174, stabilizing the protein and inducing transcription of EIN3 target genes. In the absence of ethylene, CTR1 indirectly promotes phosphorylation of Thr 592, resulting in EIN3 degradation. An important future direction of this work will be to elucidate the proteins involved in CTR1-mediated phosphorylation of EIN3 and to clarify how CTR1 inhibits MKK9–MPK3/MPK3 signaling in the absence of ethylene. Emily J. Chenette Reference | |
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