BLANC - Blanc

Regulation of plant ethylene responses by EBF1/2-dependent turnover of EIN3 protein – EIN3-REG

Submission summary

The gas ethylene is one of the earliest characterised plant hormones. In particular the response of germinating seedlings towards ethylene, has facilitated the isolation and characterisation of many of its components using forward mutagenesis. Based on the identified mutants a detailed model of the ethylene response pathway in the model plant Arabidopsis thaliana has been built: Ethylene signal transduction begins with ethylene binding to and inactivating a family of ethylene receptors. In the absence of ethylene, these receptors activate CTR1, a mitogen activating protein kinase kinase kinase. After CTR1 inactivation, EIN2 promotes ethylene responses via the downstream transcription factor EIN3. EIN3 then activates primary targets of the ethylene response cascade. The transcription factor EIN3 has recently been shown by us and others to be regulated at the posttranslational level by the F-box proteins EBF1 and EBF2 and this regulation is of crucial importance for the vast majority of the great many developmental and growth responses to the hormone ethylene (Potuschak et al.,2003; Guo & Ecker; 2003; Gagne et al, 2004). F-box proteins are substrate binding components of ubiquitin ligating SCF complexes that target substrate proteins for proteasomal degradation (Lechner et al., 2006). In the absence of ethylene, EIN3 protein is constitutively degraded in an EBF1/2 dependent manner. However in the presence of ethylene, EIN3 is stabilised and accumulates. Likewise ebf1ebf2 mutants accumulate high levels of EIN3 protein already in the absence of ethylene and display a strong constitutive ethylene response phenotype. We previously showed that the accumulation of EIN3 positively regulates EBF1 and EBF2 mRNA levels, which presumably provides a feedback mechanism to limit the accumulation of EIN3. At the protein level ethylene dependent protein accumulation of EIN3 is completely abolished in ein2 mutant plants, reduced in ein5 and ein6 mutants, and increased in the constitutive ethylene response mutant ctr1 (Guo&Ecker, 2003). The reduced accumulation of EIN3 protein is in general matched with a reduced accumulation of EBF2 and , to a lesser extent, EBF1 transcripts in ein2, ein3 and ein6 plants whereas ctr1 plants have elevated EBF1/2 RNA levels (Potuschak et al., 2003). These sole exception to this pattern is the ein5 mutant in which reduced EIN3 accumulation is matched with moderately increased EBF1 and EBF2 levels. EIN5 was recently identified by us and others as being allelic to the cytoplasmic exoribonuclease XRN4 (Olmedo et al., 2006; Potuschak et al., 2006). While EBF1/2 mRNA levels are elevated in an ein5/xrn4 mutant background, it is unlikely that EBF1/2 mRNAs are themselves direct targets of XRN4: EBF1/2 mRNA levels remain short lived in ein5/xrn4 mutants; we and others were not able to show stabilisation of EBF1/2 mRNAs in xrn4 mutant plants (Potuschak et al., 2006, Souret et al., 2004). We therefore deem it more likely that XRN4 acts on an upstream transcriptional regulator of EBF1/2. Taken together the interdependence of EBF1/2 dependent turnover and EIN3 dependent transcription of EBF1/2 and the modulation of EBF1/2 mRNA levels by XRN4 indicates that transcriptional regulation of EBF1/2 appears to be an important and recurring theme in the regulation of EIN3 protein accumulation and in plant ethylene signalling indeed. We therefore will investigate how EBF1and 2 are transcriptionally regulated in greater detail. In particular we would like to know if EIN3 directly targets EBF1/2 promoters or if it acts through downstream components of the ethylene response cascade such as ERF1. Our interest in the transcriptional regulation of EBF1/2 has been further increased by several recent microarrray studies that show misexpression of either EBF1, EBF2 or both and in one case EIN3 itself in response to other hormones or in response to pathogens derived signals. It is widely known that different plant hormone signalling pathways int.

Project coordination

thomas POTUSCHAK (Organisme de recherche)

The author of this summary is the project coordinator, who is responsible for the content of this summary. The ANR declines any responsibility as for its contents.


Help of the ANR 225,000 euros
Beginning and duration of the scientific project: - 36 Months

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