Connections Map Overview

The Canonical Ethylene Signaling Pathway

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Science's STKE  24 Feb 2004:
Vol. 2004, Issue 221, pp. cm1
DOI: 10.1126/stke.2212004cm1


The structural simplicity of the plant hormone ethylene contrasts with its dramatic effects in various developmental processes, as well as in the responses to a diversity of environmental signals. This broad spectrum of responses is mediated by a single well-conserved signaling cascade. Ethylene is perceived by a family of two-component histidine kinase receptors that become inactivated upon ethylene binding. In the absence of the hormone, the receptors activate CTR1, a negative regulator of ethylene responses. Sequence similarity between CTR1 and the Raf protein kinases implies involvement of a mitogen-activated protein kinase (MAPK) cascade in this signaling pathway. The first candidate MAPKs in the ethylene response pathway have been identified. EIN2 acts downstream of CTR1 and the possible kinase cascade. Although the biochemical function of EIN2 is not understood, its critical role is manifested by the complete ethylene insensitivity of the EIN2 loss-of-function mutants. Downstream of EIN2 there is a family of plant-specific EIN3-like transcription factors that mediate all known ethylene responses. The regulation of EIN3 stability by ethylene is accomplished by F-box-containing proteins that participate in the formation of a SCF complex, which targets proteins for degradation by the proteasome. A large number of ethylene-regulated genes have been identified, among them the AP2-domain containing ERF1 and EDF family of transcription factors, which suggests the participation of a transcriptional cascade in the ethylene response. The differential regulation of some components of this complex nuclear cascade by other signaling pathways provides a possible mechanism for interaction and signal integration. As new points of intersection with other pathways and additional participants in the pathway are identified, the Connections Map will be updated to include this new information.

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