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

Invertebrate Survival Journal

卷:13

LC Smith¹  MR Coscia² 

[1] Department of Biological Sciences, George Washington University, Washington DC, USA;

[2] Institute of Protein Biochemistry, National Research Council of Italy, Naples, Italy;

关键词: Ig;    TcR;    VLR;    DSCAM;    FREPs;    VCBP;    TLR;    Fu/HC;    R genes;    Sp185/333;   

DOI  :  

来源: DOAJ

【 摘 要 】

Diversification of immune genes in host organisms that are in deadly arms races with pathogenshas resulted in a wide range of approaches by which the host survives. Well known examples ofadaptive immunity in vertebrates include somatic recombination of the immunoglobulin gene familyand assembly of the variable lymphocyte receptors. The CRISPR-Cas system in bacteria and archaeais also considered adaptive. For invertebrates that survive in the absence of adaptive immunity, innateimmune 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 extensivealternative splicing or increases in alleles in populations. The Sp185/333 gene family in the purple seaurchin has multiple levels in which to generate immune diversity. These include clustered Sp185/333genes, genomic instability in regions harboring the genes, predicted mRNA editing, expression ofbroad repertoires of Sp185/333 proteins, and post translational modifications. The Sp185/333 proteinshave anti-pathogen activities and an individual recombinant protein can bind to multiple foreign cellsand molecular patterns. The underlying characteristics of gene clusters, many with repeats, that arepresent in unstable genomic regions is common to a number of these examples, and is likely of centralimportance for organisms that survive solely on innate immunity.

【 授权许可】

Unknown