Hypothesis: biological role for J-C intronic matrix attachment regions in the molecular mechanism of antigen-driven somatic hypermutation.
A major function of J-C intronic matrix attachment regions (MAR) during immune diversification via somatic hypermutation (SHM) at immunoglobulin loci may be to manipulate the topology of DNA within the upstream target domain. The suggestion that SHM induction requires MAR-induced torsional strain, in conjunction with DNA remodelling at the J-C intron, completes the definition of a cogent paradigm within which all extant molecular data on the issue may be interpreted. Moreover, the suggestion that a mutagenic mechanism relieves MAR-generated superhelicity could provide an indication as to the evolutionary basis of SHM.
Franklin
Andrew
A
Division of Immunology and Genetics, The John Curtin School of Medical Research, Australian National University, Canberra, Australian Capital Territory, Australia. Andrew.Franklin@anu.edu.au
Blanden
Robert V
RV
D000941:Antigens / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology / Q000378:metabolism; D015322:Gene Rearrangement, B-Lymphocyte / Q000235:genetics; D007438:Introns / Q000235:genetics*; D045170:Matrix Attachment Regions / Q000235:genetics*; D008957:Models, Genetic; D018448:Models, Immunological; D009690:Nucleic Acid Conformation; D027041:Somatic Hypermutation, Immunoglobulin / Q000235:genetics* / Q000276:immunology*
D000941:Antigens