|ZFIN ID: ZDB-PUB-180224-1|
Whole genome duplications have provided teleosts with many roads to peptide loaded MHC class I molecules
|Source:||BMC Evolutionary Biology 18: 25 (Journal)|
|Keywords:||Antigen presentation, MHC, Peptide loading complex, Phylogeny, Salmonids, Teleosts|
|PubMed:||29471808 Full text @ BMC Evol. Biol.|
Grimholt, U. (2018) Whole genome duplications have provided teleosts with many roads to peptide loaded MHC class I molecules. BMC Evolutionary Biology. 18:25.
Background In sharks, chickens, rats, frogs, medaka and zebrafish there is haplotypic variation in MHC class I and closely linked genes involved in antigen processing, peptide translocation and peptide loading. At least in chicken, such MHCIa haplotypes of MHCIa, TAP2 and Tapasin are shown to influence the repertoire of pathogen epitopes being presented to CD8+ T-cells with subsequent effect on cell-mediated immune responses.
Results Examining MHCI haplotype variation in Atlantic salmon using transcriptome and genome resources we found little evidence for polymorphism in antigen processing genes closely linked to the classical MHCIa genes. Looking at other genes involved in MHCI assembly and antigen processing we found retention of functional gene duplicates originating from the second vertebrate genome duplication event providing cyprinids, salmonids, and neoteleosts with the potential of several different peptide-loading complexes. One of these gene duplications has also been retained in the tetrapod lineage with orthologs in frogs, birds and opossum.
Conclusion We postulate that the unique salmonid whole genome duplication (SGD) is responsible for eliminating haplotypic content in the paralog MHCIa regions possibly due to frequent recombination and reorganization events at early stages after the SGD. In return, multiple rounds of whole genome duplications has provided Atlantic salmon, other teleosts and even lower vertebrates with alternative peptide loading complexes. How this affects antigen presentation remains to be established.