1. ¹Institute of Microbiology, University of Lausanne, Lausanne, Switzerland
2. ²Center of Integrative Genomics, University of Lausanne, Lausanne, Switzerland
3. ³Laboratory of Molecular Immunology, US Army Medical Research Institute of Infectious Diseases, Frederick, MD, USA
4. ⁴Cancer and Inflammation Program, Laboratory of Experimental Immunology, SAIC-Frederick Inc., NCI–Frederick, Frederick, MD, USA
5. ⁵Institut Pasteur, Human Evolutionary Genetics, CNRS, URA3012, Paris, France

Correspondence: Professor A Telenti, Institute of Microbiology, Centre Hospitalier Univeritaire Vaudois, Bugnon 48, CHUV, Lausanne 1011, Switzerland. E-mail: amalio.telenti@chuv.ch

Received 2 April 2008; Revised 24 April 2008; Accepted 25 April 2008; Published online 5 June 2008.

Abstract

The CD209 gene family that encodes C-type lectins in primates includes CD209 (DC-SIGN), CD209L (L-SIGN) and CD209L2. Understanding the evolution of these genes can help understand the duplication events generating this family, the process leading to the repeated neck region and identify protein domains under selective pressure. We compiled sequences from 14 primates representing 40 million years of evolution and from three non-primate mammal species. Phylogenetic analyses used Bayesian inference, and nucleotide substitutional patterns were assessed by codon-based maximum likelihood. Analyses suggest that CD209 genes emerged from a first duplication event in the common ancestor of anthropoids, yielding CD209L2 and an ancestral CD209 gene, which, in turn, duplicated in the common Old World primate ancestor, giving rise to CD209L and CD209. K_A/K_S values averaged over the entire tree were 0.43 (CD209), 0.52 (CD209L) and 0.35 (CD209L2), consistent with overall signatures of purifying selection. We also assessed the Toll-like receptor (TLR) gene family, which shares with CD209 genes a common profile of evolutionary constraint. The general feature of purifying selection of CD209 genes, despite an apparent redundancy (gene absence and gene loss), may reflect the need to faithfully recognize a multiplicity of pathogen motifs, commensals and a number of self-antigens.