Abstract
Antibody diversification by somatic hypermutation, gene conversion, and class switch recombination is completely dependent on activation-induced cytidine deaminase (AID). A recent report showing induction of DNA mutations in Escherichia coli by overexpression of AID, Apobec-1, and related members of the RNA-editing cytidine deaminase family suggested that they may directly modify deoxycytidine in DNA in mammalian cells (DNA-editing model). We therefore examined whether Apobec-1 bona fide RNA-editing enzyme could show somatic hypermutation and class switching activities in murine B lymphocytes and fibroblasts. Unlike AID, Apobec-1 was unable to induce somatic hypermutation or class switching. The results force a reevaluation of the physiological significance of the DNA deaminase activities of AID and Apobec-1 in E. coli and in vitro.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
3T3 Cells
-
APOBEC-1 Deaminase
-
Animals
-
Apolipoproteins B / genetics*
-
Apolipoproteins B / immunology
-
B-Lymphocytes / immunology
-
B-Lymphocytes / physiology
-
Cell Line
-
Cloning, Molecular
-
Cytidine Deaminase / genetics*
-
Cytidine Deaminase / immunology
-
Escherichia coli / genetics
-
Escherichia coli / immunology
-
Genes, Reporter
-
Green Fluorescent Proteins
-
Luminescent Proteins / genetics
-
Mammals
-
Mice
-
Mutagenesis
-
RNA Editing / genetics*
-
RNA Editing / immunology
-
RNA, Messenger / genetics
-
Recombinant Proteins / immunology
-
Somatic Hypermutation, Immunoglobulin / genetics
-
Somatic Hypermutation, Immunoglobulin / immunology*
-
Transcription, Genetic
Substances
-
Apolipoproteins B
-
Luminescent Proteins
-
RNA, Messenger
-
Recombinant Proteins
-
Green Fluorescent Proteins
-
APOBEC-1 Deaminase
-
Apobec1 protein, mouse
-
Cytidine Deaminase