Complementation of V(D)J recombination deficiency in RAG-1(-/-) B cells reveals a requirement for novel elements in the N-terminus of RAG-1

Immunity. 1997 Jul;7(1):13-24. doi: 10.1016/s1074-7613(00)80506-3.


RAG-1 is an essential component of the site-specific V(D)J recombinase. A new assay system has revealed a significant contribution of the catalytically dispensible N-terminal region of RAG-1 to recombination activity. The foundation for this system is an Abelson virus-transformed cell line derived from RAG-1(-/-) mice that is dependent on the introduction of exogenous RAG-1 for rearrangement of either plasmid substrates or the endogenous immunoglobulin loci. Use of this line demonstrates that conserved and novel cysteine-containing elements in the N-terminal region are required for full RAG-1 activity when recombination activity is in a RAG-1 dose-responsive range. Our data suggest that the RAG-1 N-terminus enhances the formation of an active recombination complex that facilitates the rearrangement process.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Abelson murine leukemia virus
  • Amino Acid Sequence
  • Animals
  • B-Lymphocytes / metabolism*
  • Binding Sites
  • Catalysis
  • Cell Transformation, Viral
  • Chromosome Mapping
  • Consensus Sequence
  • Cysteine / metabolism
  • DNA Nucleotidyltransferases / metabolism*
  • DNA-Binding Proteins / chemistry
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / physiology*
  • Gene Rearrangement, B-Lymphocyte / genetics*
  • Genes, RAG-1*
  • Homeodomain Proteins*
  • Mice
  • Molecular Sequence Data
  • VDJ Recombinases


  • DNA-Binding Proteins
  • Homeodomain Proteins
  • RAG-1 protein
  • DNA Nucleotidyltransferases
  • VDJ Recombinases
  • Cysteine