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Review
. 2015 Sep;169(1):32-41.
doi: 10.1104/pp.15.00677. Epub 2015 Jun 23.

Ethylene Response Factors: A Key Regulatory Hub in Hormone and Stress Signaling

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Free PMC article
Review

Ethylene Response Factors: A Key Regulatory Hub in Hormone and Stress Signaling

Maren Müller et al. Plant Physiol. .
Free PMC article

Abstract

Ethylene is essential for many developmental processes and a key mediator of biotic and abiotic stress responses in plants. The ethylene signaling and response pathway includes Ethylene Response Factors (ERFs), which belong to the transcription factor family APETALA2/ERF. It is well known that ERFs regulate molecular response to pathogen attack by binding to sequences containing AGCCGCC motifs (the GCC box), a cis-acting element. However, recent studies suggest that several ERFs also bind to dehydration-responsive elements and act as a key regulatory hub in plant responses to abiotic stresses. Here, we review some of the recent advances in our understanding of the ethylene signaling and response pathway, with emphasis on ERFs and their role in hormone cross talk and redox signaling under abiotic stresses. We conclude that ERFs act as a key regulatory hub, integrating ethylene, abscisic acid, jasmonate, and redox signaling in the plant response to a number of abiotic stresses.

Figures

Figure 1.
Figure 1.
Model of the ethylene (ET) signaling pathway to ERFs. In the absence of ethylene (left), the ethylene receptors promote CTR1 kinase activity, resulting in the phosphorylation of the C-terminal domain of EIN2. Because of the protein turnover involving the F-box proteins ETP1/2 and EBF1/2, the protein levels of both EIN2 and EIN3/EIL1 are extremely low. In the presence of ethylene (right), the inactivation of the ethylene receptors and CTR1 results in the dephosphorylation and cleavage of the EIN2 C terminus and translocation to the nucleus, where they regulate EIN3/EIL1 activation directly or indirectly. The direct targets of EIN3 are the TF genes ERFs, such as ERF1, which activates, depending on the stress conditions (either biotic [pathogen infection] or abiotic [e.g. dehydration, salinity, or heat shock] stress), a specific set of stress response genes by binding to the specific cis-acting GCC box and DRE elements. ER, Endoplasmic reticulum; ECIP1, EIN2 C-TERMINUS INTERACTING PROTEIN1.
Figure 2.
Figure 2.
Proposed model for ethylene (ET), jasmonic acid (JA), and ABA cross talk through ERFs under abiotic stress. ERF1 induces expression of genes involved in abiotic stress tolerance. It has been postulated that, through the activation of JERF1 and TSRF1 (ERFs from the same ERF subfamily), ERF1 activates expression of NtSDR, an ABA biosynthesis-related gene. In turn, ABA might down-regulate ERF1 expression under abiotic stress. However, the negative effect of ABA does not seem to block ET/JA signaling. LEA4-5, Late-Embryogenesis Abundant Protein4-5; HSFA3, Heat-Shock Transcription Factor A3; HSP101, Heat-Shock Protein101.
Figure 3.
Figure 3.
Proposed model for ROS signaling to ERFs. Biotic and abiotic stresses enhance ROS production, resulting in the activation of MPK6, which activates ethylene biosynthesis by phosphorylation of ACS6. Then, EIN2, EIN3/EIL1, and finally, ERF1 are activated, which could result in the activation of ROS gene expression that enhances stress tolerance. Recently, it has been suggested that ERF6 is activated by MPK6 phosphorylation independently of EIN3/EIL1 under oxidative stress.

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