title: Patterns of evolutionary selection pressure in the immune signaling protein TRAF3IP2 in mammals.
abstract: TRAF3 interacting protein 2 (TRAF3IP2) is important for immune responses to pathogens, inflammatory signals and autoimmunity in mammals. In the present study, we collected 19 mammalian TRAF3IP2 sequences and investigated the various types of selection pressure acting on them. Maximum likelihood estimations of nonsynonymous (dN) to synonymous (dS) substitution (dN/dS) ratios for the aligned coding sequences indicated that, as a whole, TRAF3IP2 has been subject to purifying selection. However, the N-terminus of the protein has been subject to higher selection pressure than the C-terminal domain. While eight amino acid residues within the N-terminus appear to have evolved under positive selection, no evidence for such selection was found in the C-terminus. The positively selected residues, which fall outside the currently known functional sites within TRAF3IP2, may have novel functions. The different selection pressures acting on the N- and C-terminal regions are consistent with their protein structures: the C-terminal structure is an ordered structure, whereas the N-terminus is disordered. Taken together with the results of previous studies, it is plausible that positive selection on the N-terminus of TRAF3IP2 may have occurred by competitive coevolution between mammalian hosts and viruses.
authors.affiliation: Department of Biological Sciences, Wayne State University, 5047 Gullen Mall, Detroit, MI 48202, USA.
authors.forename: Baojun
authors.initials: B
authors.lastname: Wu
authors.forename: Jing
authors.initials: J
authors.lastname: Gong
authors.forename: Shoudao
authors.initials: S
authors.lastname: Yuan
authors.forename: Ying
authors.initials: Y
authors.lastname: Zhang
authors.forename: Tiandi
authors.initials: T
authors.lastname: Wei
mesh_terms: D048868:Adaptor Proteins, Signal Transducing; D000818:Animals; D002417:Cattle; D019143:Evolution, Molecular; D006168:Guinea Pigs; D054884:Host-Pathogen Interactions / Q000235:genetics / Q000276:immunology; D006801:Humans; D007109:Immunity / Q000235:genetics*; D008322:Mammals / Q000235:genetics* / Q000276:immunology; D051379:Mice; D008958:Models, Molecular; D011817:Rabbits; D051381:Rats; D012641:Selection, Genetic; D015398:Signal Transduction / Q000235:genetics / Q000276:immunology; D047988:Tumor Necrosis Factor Receptor-Associated Peptides and Proteins / Q000737:chemistry / Q000235:genetics*
chemical_list: D048868:Adaptor Proteins, Signal Transducing; C414202:TRAF3IP2 protein, human; D047988:Tumor Necrosis Factor Receptor-Associated Peptides and Proteins
keywords: Adaptive evolution; B-cell-activating factor receptor; BAFFR; CC; CIKS; Competitive coevolution; FEL; FUBAR; HLH; IDR; IKKi; IL17R; Immune defense; IκB kinase I; MEME; Mammalian TRAF3IP2; NF-κB; NG; NJ; Nei–Gojobori; SAPK/JNK; SEF/interleukin 17 receptor; SEFIR; SLAC; TIR; TNF receptor associated factor 3 interacting protein 2; TNF receptor associated factor 6; TRAF3IP2; TRAF6; Toll/interleukin 1 receptor; coiled-coil; dN/dS; fast unconstrained Bayesian approximation; fixed effects likelihood; helix–loop–helix; interleukin 17 receptor; intrinsically disordered region; mixed effects model of evolution; neighbor-joining; nonsynonymous/synonymous substitution rate ratio; nuclear factor-kappa B; single likelihood ancestor counting