Alternative Splicing of SCL30a Generates Distinct Isoforms to Modulate ABA Signaling in Arabidopsis

Alternative splicing (AS) coupled with nonsense-mediated decay (NMD) is an important post-transcriptional mechanism that regulates the expression of many genes, including serine/arginine-rich (SR) proteins across eukaryotes. In plants, SR proteins participate in diverse developmental processes and stress responses, particularly in abscisic acid (ABA) signaling. However, the functional differences among individual splice isoforms of SR proteins remain poorly understood. Here, we investigated SCL30a, a plant-specific SR protein in Arabidopsis thaliana. By integrating third-generation long-read transcriptome sequencing, NMD stability assays, and subcellular localization analyses, we identified five alternatively spliced SCL30a transcripts. Among them, SCL30a.2 and SCL30a.3 contain premature termination codons (PTCs), display nucleocytoplasmic localization, and are rapidly degraded through the NMD pathway. In contrast, the other three isoforms, SCL30a.1, SCL30a.4, and SCL30a.5, retain an intact RS domain and localize exclusively to the nucleus. Functional analyses showed that SCL30a acts as a positive regulator of ABA signaling. Loss-of-function mutants of SCL30a displayed reduced ABA sensitivity in both root growth and seed germination assays, whereas complementation or overexpression of three stable isoforms of SCL30a (SCL30a.1, SCL30a.4, and SCL30a.5) enhanced ABA responsiveness. Transcriptome analysis further showed that the expression of a subset of ABA-related genes, particularly SnRK2.6, was significantly altered in ABA-treated scl30a mutants and SCL30a.1-OE lines compared with WT plants. In addition, genetic evidence showed that overexpression of SnRK2.6 rescued the ABA-insensitive phenotype of the scl30a mutant. Together, these findings suggest that SnRK2.6 may function as a candidate downstream component associated with SCL30a-mediated ABA responses.