Tuning the host-pathogen relationship through evolution with a special focus on the echinoid Sp185/333 system

Abstract

Diversification of immune genes in host organisms that are in deadly arms races with pathogens has resulted in a wide range of approaches by which the host survives. Well known examples of adaptive immunity in vertebrates include somatic recombination of the immunoglobulin gene family and assembly of the variable lymphocyte receptors. The CRISPR-Cas system in bacteria and archaea is also considered adaptive. For invertebrates that survive in the absence of adaptive immunity, innate immune diversity is accomplished based on functions of clusters of immune genes such as FREPs, VCBPs, C1qs, TLRs, and R genes. Single copy gene diversity can be accomplished through extensive alternative splicing or increases in alleles in populations. The Sp185/333 gene family in the purple sea urchin has multiple levels in which to generate immune diversity. These include clustered Sp185/333 genes, genomic instability in regions harboring the genes, predicted mRNA editing, expression of broad repertoires of Sp185/333 proteins, and post translational modifications. The Sp185/333 proteins have anti-pathogen activities and an individual recombinant protein can bind to multiple foreign cells and molecular patterns. The underlying characteristics of gene clusters, many with repeats, that are present in unstable genomic regions is common to a number of these examples, and is likely of central importance for organisms that survive solely on innate immunity.