YTHDC1, a nuclear m⁶A reader, regulates mRNA splicing by promoting exon inclusion through the recruitment of SRSF3 while blocking SRSF10 binding to mRNAs. This study shows that YTHDC1 competitively binds to SRSF3 and SRSF10, with SRSF3 facilitating exon inclusion and SRSF10 promoting exon skipping. PAR-CLIP-seq analysis revealed that YTHDC1-regulated exon-inclusion patterns are similar to those of SRSF3 but opposite of SRSF10. In vitro pull-down assays demonstrated competitive binding of SRSF3 and SRSF10 to YTHDC1. YTHDC1 enhances SRSF3 but represses SRSF10 in nuclear speckle localization, RNA-binding affinity, and splicing events. Depletion of YTHDC1 leads to dysregulation of splicing, which can be restored by reconstitution with wild-type, but not m⁶A-binding-defective, YTHDC1. These findings provide direct evidence that YTHDC1 regulates mRNA splicing by recruiting and modulating pre-mRNA splicing factors for their access to the binding regions of targeted mRNAs. The study highlights the role of YTHDC1 in bridging trans- and cis-regulatory elements to regulate mRNA splicing.YTHDC1, a nuclear m⁶A reader, regulates mRNA splicing by promoting exon inclusion through the recruitment of SRSF3 while blocking SRSF10 binding to mRNAs. This study shows that YTHDC1 competitively binds to SRSF3 and SRSF10, with SRSF3 facilitating exon inclusion and SRSF10 promoting exon skipping. PAR-CLIP-seq analysis revealed that YTHDC1-regulated exon-inclusion patterns are similar to those of SRSF3 but opposite of SRSF10. In vitro pull-down assays demonstrated competitive binding of SRSF3 and SRSF10 to YTHDC1. YTHDC1 enhances SRSF3 but represses SRSF10 in nuclear speckle localization, RNA-binding affinity, and splicing events. Depletion of YTHDC1 leads to dysregulation of splicing, which can be restored by reconstitution with wild-type, but not m⁶A-binding-defective, YTHDC1. These findings provide direct evidence that YTHDC1 regulates mRNA splicing by recruiting and modulating pre-mRNA splicing factors for their access to the binding regions of targeted mRNAs. The study highlights the role of YTHDC1 in bridging trans- and cis-regulatory elements to regulate mRNA splicing.