Fig. 4

Immunogenomic basis of asplenia and male pregnancy in seahorses.

a Copy numbers of key genes involved in the development and function of DC, MHC, T/B lymphocytes, and complement components 3–4 in seahorses and other vertebrates. DC dendritic cell, MHC major histocompatibility complex. *, variation of ITAM (immunoreceptor tyrosine-based activation motif) region; †, based on partial sequence (low-coverage sequencing and genome assemblies), but featuring the variation of ITAM; #, Total number of MHC II. The brood pouch types are shown on the right. Hippocampus and Syngnathus species exhibit the closed brood pouches. b Schematic map illustrating the hypothesized molecular trade-offs in the male pregnancy of seahorses. Asplenia caused by the tlx1 mutation could decrease the CD5⁺ B cell populations. In addition to the corresponding reduced diversity in antibodies, the classical complement pathway triggered by antibody-antigen-interactions might also be weakened, affecting the downstream events usually triggering allograft rejection. Loss of C4 is expected to be associated with decreased abundance of Treg cells, which orchestrate self-immune tolerance. The shaded icon and dotted line indicate gene loss in seahorse genomes. Treg cell, regulatory T cell. The figures were created with BioRender.com.