OsMED25-OsWRI1 Fine-Tunes Fatty Acid Biosynthesis: A Key Strategy via Intron Retention

In rice grains, the mechanisms governing fatty acid biosynthesis remain largely elusive. Although WRINKLED1 (WRI1) is well established as a core transcription factor activating fatty acid biosynthesis under multi-level regulation, its post-transcriptional regulation has been scarcely explored. Here, we demonstrate that OsWRI1 transcripts undergo alternative splicing (AS) via intron retention (IR), producing two functionally distinct splice variants: OsWRI1α and OsWRI1β. OsWRI1α encodes a canonical protein containing two AP2 domains, whereas OsWRI1β produces a truncated protein due to a premature termination codon. Genetic analyses confirm that OsWRI1α functions as a positive regulator of fatty acid biosynthesis, while OsWRI1β exerts an inhibitory effect by directly interacting with OsWRI1α, disrupting its dimerization, and preventing activation of downstream target genes including OsACP1 and OsFAD2. We further identify OsMED25 as a critical regulator of this AS event. OsMED25 is recruited to a 360-bp intronic region of OsWRI1 that corresponds precisely to the retained intron in OsWRI1β, where it recruits the splicing factor OsPTB4 to promote intron retention, thereby repressing fatty acid biosynthesis. The induction of OsWRI1β expression by jasmonic acid (JA) signaling, which we identify as a suppressor of fatty acid biosynthesis, is strictly dependent on OsMED25. Mechanistically, JA enhances OsMED25 protein stability and promotes its association with OsWRI1 pre-mRNA. Together, these findings establish that IR-mediated AS of OsWRI1 defines a regulatory mechanism where the JA-OsMED25-OsPTB4-OsWRI1 axis coordinates carbon flux and energy homeostasis during grain lipid accumulation. Thus, OsMED25 integrates upstream JA signaling to fine-tune OsWRI1 splicing, modulating fatty acid biosynthesis during rice grain development.