Characterization of the type I subgroup d IFN gene locus in large yellow croaker (larimichthys crocea) reveals a transposition-associated mechanism of type I IFN gene expansion in teleosts.

Type I interferons (IFNs) are key innate immune cytokines and have undergone extensive lineage-specific gene expansion during vertebrate evolution. Although IFN gene expansion has traditionally been attributed to local tandem duplication, whether alternative genomic mechanisms contribute to the diversification of type I IFN genes remains largely unexplored. Here, we identified an unusual expansion pattern of the type I subgroup d IFN gene (IFNd) in the large yellow croaker (Larimichthys crocea, Lc), revealing a potential transposition-associated mechanism underlying the duplication and relocation of an intron-containing type I IFN genomic module. Comparative genomic analyses suggest that IFNd genes in all fish species examined are conserved at the immunoglobulin-associated beta (CD79b)-pleckstrin homology and RUN domain containing M1 protein (PLEKHM1) locus, whereas sciaenid species possess an additional head-to-head IFNd pair within the F-box and WD repeat-containing protein (FBXW10)-PR/SET domain 9 (PRDM9) intergenic region. Phylogenetic analyses indicate that these duplicated copies originated from the ancestral sciaenid IFNd clade. The additional IFNd locus retains the conserved IFNd genomic architecture, including gene organization, intron-exon structure, and flanking genomic elements, supporting the duplication and relocation of an intact IFNd-containing module. The presence of repetitive sequences near the inserted locus further suggests that genome rearrangement-associated processes may have contributed to the expansion event. Molecular dating suggests that the emergence of the additional IFNd module occurred after the divergence of sciaenids from other percomorph lineages but before diversification of extant sciaenid species. The present study thus provides evidence supporting the hypothesis that transposition-associated duplication and long-range relocation of intact IFN genomic modules represent an additional mechanism contributing to type I IFN gene expansion in teleosts.