Male infertility is an increasingly pressing global health concern, with abnormal spermiogenesis being a major cause of asthenoteratozoospermia. Although RNA-binding proteins (RBPs)-orchestrated alternative splicing has recently garnered significant attention, its regulation mechanisms during spermiogenesis remain unclear. Here, we identify hnRNPR as a crucial m6A-dependent splicing regulator. Mutations in hnRNPR lead to asthenoteratozoospermia in both humans and mice. Mechanistically, loss of hnRNPR exhibits widespread transcriptomic, proteomics, and m6A-modified splicing dysregulation, disrupting these genes essential for acrosome formation and flagellum development. Remarkably, Skap2 knockdown mice exhibit sperm defects that phenocopy those seen in Hnrnpr mutants. Importantly, therapeutic delivery of SKAP2, via extracellular vesicles, restores F-actin-mediated cytoskeletal integrity and improves sperm motility. Collectively, these findings establish that spermiogenesis is controlled post-transcriptionally by splicing in an m6A-dependent manner and reveal a promising therapeutic contribution for male infertility.