Indels and imperfect duplication have driven the evolution of human Complement Receptor 1 (CR1) and CR1-like from their precursor CR1 alpha: importance of functional sets

Hum Immunol. 2005 Mar;66(3):258-73. doi: 10.1016/j.humimm.2005.01.004.

Abstract

This study examines the effects of duplication and insertions-deletions (indels) by comparing human complement receptor 1 (CR1) and human CR1-like (CR1L) with syntenic genes from four other vertebrates (chimpanzee, baboon, rat, and mouse). By phylogenetic analysis, the domains of these genes can be classified into 10 distinct subfamilies (a, b, c, d, e, f, g(-like), h, j, and k), which have been largely conserved throughout vertebrate and invertebrate evolution. In spite of many complex and diverse duplications and indels, the subfamily order of domains (a, j, e, f, b, k, d, g(-like)) has been maintained. The number of domain sets has increased progressively, thereby expanding the functional repertoire.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Antigens, Surface
  • Evolution, Molecular*
  • Gene Duplication*
  • Humans
  • Mice
  • Molecular Sequence Data
  • Multigene Family
  • Pan troglodytes / genetics
  • Papio cynocephalus / genetics
  • Papio hamadryas / genetics
  • Rats
  • Receptors, Cell Surface
  • Receptors, Complement / genetics*
  • Receptors, Complement 3b / genetics*
  • Sequence Alignment

Substances

  • Antigens, Surface
  • CR1L protein, human
  • Cr1l protein, mouse
  • Cr1l protein, rat
  • Receptors, Cell Surface
  • Receptors, Complement
  • Receptors, Complement 3b