Figure 7.

Revisited model for ACC/ethylene biosynthesis and signaling. (A) ACC/ethylene signaling pathway in normal conditions, where the responses are mainly mediated by ethylene. A major portion of ACC is converted to ethylene by ACO. The signal is then transferred via key signaling components ultimately leading to ethylene responses. The remaining ACC is transported to other tissues, conjugated to storage forms or perceived by (a) putative ACC receptor(s). Subsequent ACC responses are assumed to be minimal. (B) ACC/ethylene signaling pathway in conditions where ACC accumulates and leads to ACC-specific responses. ACC accumulation can result from an inhibition of ACO by inhibitors (e.g., AIB; shown in red), saturation of ACO activity (leading to overflow), or any other inhibition of ACO caused by internal or external signals. Elevated levels of ACC bind to its receptor(s), activating unidentified downstream components, ultimately leading to ACC-specific responses. Alternatively, ACC could, upon interaction with its receptor(s) act via EIN2, activating ethylene-mediated gene expression, while bypassing the need for ethylene perception. Additionally, the ACO inhibitor AIB potentially affects other ACC binding proteins such as putative receptors, transporters or conjugating enzymes. Arrow-headed lines represent stimulatory interactions. Bar-headed lines represent inhibitory interactions. Thick lines depict the predominantly active pathway. Dashed lines indicated relations that have not been demonstrated experimentally. 1-MCP, 1-methylcyclopropene; ACC, 1-aminocyclopropane-1-carboxylic acid; ACO, ACC oxidase; ACS, ACC synthase; AIB, 2-aminoisobutyric acid; CTR, constitutive triple response; ETR, ethylene response; ERS, ethylene response sensor; EIN, ethylene insensitive; EIL, EIN3-like.