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Published December 1, 2006 | Supplemental Material
Journal Article Open

The immune gene repertoire encoded in the purple sea urchin genome

Abstract

Echinoderms occupy a critical and largely unexplored phylogenetic vantage point from which to infer both the early evolution of bilaterian immunity and the underpinnings of the vertebrate adaptive immune system. Here we present an initial survey of the purple sea urchin genome for genes associated with immunity. An elaborate repertoire of potential immune receptors, regulators and effectors is present, including unprecedented expansions of innate pathogen recognition genes. These include a diverse array of 222 Toll-like receptor (TLR) genes and a coordinate expansion of directly associated signaling adaptors. Notably, a subset of sea urchin TLR genes encodes receptors with structural characteristics previously identified only in protostomes. A similarly expanded set of 203 NOD/NALP-like cytoplasmic recognition proteins is present. These genes have previously been identified only in vertebrates where they are represented in much lower numbers. Genes that mediate the alternative and lectin complement pathways are described, while gene homologues of the terminal pathway are not present. We have also identified several homologues of genes that function in jawed vertebrate adaptive immunity. The most striking of these is a gene cluster with similarity to the jawed vertebrate Recombination Activating Genes 1 and 2 (RAG1/2). Sea urchins are long-lived, complex organisms and these findings reveal an innate immune system of unprecedented complexity. Whether the presumably intense selective processes that molded these gene families also gave rise to novel immune mechanisms akin to adaptive systems remains to be seen. The genome sequence provides immediate opportunities to apply the advantages of the sea urchin model toward problems in developmental and evolutionary immunobiology.

Additional Information

© 2006 Elsevier Inc. Received for publication 1 June 2006; revised 21 August 2006; accepted 28 August 2006. Available online 3 September 2006. J.P.R. is supported by grants from the Canadian Institutes of Health Research (CIHR) and the National Science and Engineering Research Council of Canada (NSERC). L.C.S. is supported by a grant from the National Science Foundation (MCB04-24235). This work was in part supported by the Intramural Research Program of the National Institute on Aging/National Institutes of Health to S.D.F. T.H. is supported by a Fellowship for Research Abroad from the Uehara Memorial Foundation. We are grateful to D.J. Philpott, S.E. Girardin and D. Filipp (University of Toronto), G. W. Litman (University of South Florida), L. DuPasquier (University of Basel) and E.V. Rothenberg (Caltech) for the enlightening discussions.

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