PUBLICATION

Identification of the activation-induced cytidine deaminase gene from zebrafish: an evolutionary analysis

Authors
Zhao, Y., Pan-Hammarstrom, Q., Zhao, Z., and Hammarstrom, L.
ID
ZDB-PUB-040826-4
Date
2005
Source
Developmental and comparative immunology   29(1): 61-71 (Journal)
Registered Authors
Zhao, Yaofeng
Keywords
Activation-induced cytidine deaminase; Class switch recombination; C-terminal; Deaminase motif; Evolution; Genomic structure; Somatic hypermutation; Zebrafish AID(AICDA), activation-induced cytidine deaminase; CSR, class switch recombination; HIGM, hyper-IgM syndrome; RACE, rapid amplification of cDNA ends; SHM, somatic hypermutation
MeSH Terms
  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Cloning, Molecular
  • Conserved Sequence
  • Cytidine Deaminase/genetics
  • Cytidine Deaminase/metabolism*
  • Dogs
  • Evolution, Molecular*
  • Immunoglobulin Class Switching
  • Molecular Sequence Data
  • Pan troglodytes
  • Phylogeny
  • Sequence Homology, Amino Acid
  • Zebrafish/genetics
  • Zebrafish/metabolism*
PubMed
15325524 Full text @ Dev. Comp. Immunol.
Abstract
In the present study, we report the identification of the activation-induced cytidine deaminase (AID) encoding gene in frog, dog and chimpanzee, where both somatic hypermutation and class switch recombination (CSR) occurs and in zebrafish and fugu, species lacking CSR. The cDNA sequence of the zebrafish AID reported here suggests both N and C ends of the previously predicted protein sequence are incorrect. A comparison of AID sequences among mammals, birds, amphibians and fish revealed conserved aa residues which may be essential for AID activity, although the cytidine deaminase active motif in the latter is nine amino acids longer. Furthermore, an aa deletion, and extensive substitutions in the C terminal end of AID from bony fish indicate that the molecule may not yet have developed a capacity to recruit the specific cofactor(s) needed to initiate CSR.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping