SKIP Regulates ABA Signaling through Alternative Splicing in Arabidopsis

Abscisic acid (ABA) plays key roles in plant development and responses to abiotic stresses. A wide number of transcriptional and posttranslational regulatory mechanisms of ABA signaling are known; however, less is known about the regulatory roles of alternative splicing. In this work, we found that SKIP, a splicing factor, positively regulates ABA signaling. SKIP binds to the pre-mRNA of ABA signaling-related genes, such as PYL7, PYL8, ABI1, HAB1 and ABI5, to regulate their splicing. The precursor mRNA alternative splicing of several PYL receptors, PP2C phosphatases and ABF transcriptional factors is disrupted by the skip-1 mutation. The abnormal alternative splicing in skip-1 represses the expression of ABA-positive regulators, including PYLs and ABFs, and activates the expression of ABA-negative regulators, such as PP2Cs, which confers ABA hyposensitive phenotype of skip-1. We also found that ABA-mediated genome-wide alternative splicing and differential gene expression are changed by the skip-1 mutation. The number of the differential splicing events is increased by skip-1; however, the number of differential expressed genes in response to ABA is reduced by skip-1. Our results reveal a principle on how a splicing factor regulates ABA signaling and ABA-mediated genome-wide alternative splicing.