Convergent Evolution Within CEA Gene Families in Mammals: Hints for Species-Specific Selection Pressures
At the genetic level, one of the fastest means to adapt to environmental cues is by gene duplication. Gene duplication is the core process of gene family evolution, which is described by a model called birth-and-death evolution. According to this model, t
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Convergent Evolution Within CEA Gene Families in Mammals: Hints for Species-Specific Selection Pressures Robert Kammerer, Florian Herse and Wolfgang Zimmermann
Abstract At the genetic level, one of the fastest means to adapt to environmental cues is by gene duplication. Gene duplication is the core process of gene family evolution, which is described by a model called birth-and-death evolution. According to this model, the differences between species are more likely to be detected by comparing gene family expansion and contraction than by comparing sequences of orthologous genes. Consequently, analyzing the structure of gene families may provide deeper insight into selective pressures driving the evolution of a given species. However, tools to analyze the evolution of gene families at a larger scale are not well developed. Nevertheless, recent advances in genome sequencing provide new possibilities to characterize the evolution of gene families more comprehensively and in greater detail. Here, we describe the evolution of the carcinoembryonic antigen (CEA) gene family, which is composed of the CEA-related cell adhesion molecule (CEACAM) and the pregnancy-specific glycoprotein (PSG) gene families. We found that glycosylphosphatidylinositol (GPI)anchored CEACAMs, paired receptors, and PSG evolved independently at different time points during mammalian evolution. More specifically, we identified several features of the CEACAM/PSG gene family that are the result of convergent evolution in various mammalian species. Possible selection pressures responsible for convergent evolution and their hints toward the function of CEACAM/PSG family members are discussed.
R. Kammerer (&) Institute of Immunology, Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Greifswald-Insel, Riems, Germany e-mail: [email protected] F. Herse Experimental and Clinical Research Center, The Max-Delbrueck Center for Molecular Medicine and the Charité Medical Faculty, Berlin, Germany W. Zimmermann Tumor Immunology Laboratory, LIFE Center, University Clinic of the LMU Munich, Munich, Germany © Springer International Publishing Switzerland 2016 P. Pontarotti (ed.), Evolutionary Biology, DOI 10.1007/978-3-319-41324-2_3
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Introduction
Most multigene families were found to evolve according to a model called birth-and-death evolution. This model was first proposed in 1992 by Nei and Hughes (Nei 1992). In this model, new genes are created by gene duplication: Some of these genes are maintained and fixed in the genome, while others are deleted or become nonfunctional by deleterious mutations (Nei and Rooney 2005). Once a gene is duplicated, it may diversify to gain new functions or may only increase the gene dosage. In most cases, a functional diversification, including change in spatiotemporal expression pattern [e.g., Hox genes (Lonfat and Duboule 2015)], variation in ligand binding specificity (e.g., chemoreceptor genes (Benton 2015), or a change in signaling capacity, may occur (Sanderson et a
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