Figure 3 (IMAGE) The University of Hong Kong Caption Figure 3. Model for ACBP3/ACBP4-regulated generation of oxylipin signals during the salinity response. Under normal conditions, ACBP binding with acyl-CoAs (C18:2 and C18:3-CoAs) facilitates sequestration of an inactive lipoxygenase. High salinity triggers dissociation of this complex by a dual mechanism. First, phosphatidic acid signals compete with acyl-CoAs for ACBP binding. Second, pre-mRNAs are cut and rejoined in an unusual way (known as alternative splicing) to produce ACBP variants lacking the lipoxygenase-interacting domain. Thus, the lipoxygenase is activated to generate oxylipin signals for adaptive responses. Credit The University of Hong Kong Usage Restrictions This work is licensed for non-commercial, non-exclusive, one-time usage with attribution to the copyright holder. License Original content Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.