Figure 3 (IMAGE)
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.
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The University of Hong Kong
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