We conducted functional analysis on zebrafish mutant fn10a by polyA+, 100bp paired end, strand-specific RNA-seq. By comparing the transcriptome of fn10a mutants and their wildtype siblings or wildtype controls, we revealed a transcriptome-wide RNA splicing deficiency and a large amount of intron-retaining transcripts, which resulted in compromised nonsense-mediated RNA decay and activation of the p53 pathway in fn10a mutants. 2 biological replicates were performed to consolidate the findings. We also conducted subcellular RNA-seq between fn10a mutants and wildtype siblings, to investigate the localization of intron retaining transcripts. Overall design: The wild-type control group (WT-control group) of 36-hpf embryos was generated from mating crosses between wild-type TL zebrafish, while fn10a mutants (mutant group) and siblings (WT-sibling group) were generated from mating crosses of fn10a heterozygote zebrafish. RNA-seq of 36hpf embryos for fn10a mutants, their wildtype siblings and wildtype TL. RNA-seq of cytoplasm RNA and nuclear RNA from 36hpf embryos for fn10a mutants and their wildtype siblings.