TY - JOUR
T1 - Hypermutation of immunoglobulin genes in memory B cells of DNA repair- deficient mice
AU - Jacobs, Heinz
AU - Fukita, Yosho
AU - Van Der Horst, Gijsbertus T.J.
AU - De Boer, Jan
AU - Weeda, Geert
AU - Essers, Jeroen
AU - De Wind, Niels
AU - Engelward, Bevin P.
AU - Samson, Leona
AU - Verbeek, Sjef
AU - De Murcia, Josiane Ménissier
AU - De Murcia, Gilbert
AU - Te Riele, Hein
AU - Rajewsky, Klaus
PY - 1998/6/1
Y1 - 1998/6/1
N2 - To investigate the possible involvement of DNA repair in the process of somatic hypermutation of rearranged immunoglobulin variable (V) region genes, we have analyzed the occurrence, frequency, distribution, and pattern of mutations in rearranged Vλ1 light chain genes from naive and memory B cells in DNA repair-deficient mutant mouse strains. Hypermutation was found unaffected in mice carrying mutations in either of the following DNA repair genes: xeroderma pigmentosum complementation group (XP)A and XPD, Cockayne syndrome complementation group B (CSB), mutS homologue 2 (MSH2), radiation sensitivity 54 (RAD54), poly (ADP-ribose) polymerase (PARP), and 3- alkyladenine DNA-glycosylase (AAG). These results indicate that both subpathways of nucleotide excision repair, global genome repair, and transcription-coupled repair are not required for somatic hypermutation. This appears also to be true for mismatch repair, RAD54-dependent double-strand- break repair, and AAG-mediated base excision repair.
AB - To investigate the possible involvement of DNA repair in the process of somatic hypermutation of rearranged immunoglobulin variable (V) region genes, we have analyzed the occurrence, frequency, distribution, and pattern of mutations in rearranged Vλ1 light chain genes from naive and memory B cells in DNA repair-deficient mutant mouse strains. Hypermutation was found unaffected in mice carrying mutations in either of the following DNA repair genes: xeroderma pigmentosum complementation group (XP)A and XPD, Cockayne syndrome complementation group B (CSB), mutS homologue 2 (MSH2), radiation sensitivity 54 (RAD54), poly (ADP-ribose) polymerase (PARP), and 3- alkyladenine DNA-glycosylase (AAG). These results indicate that both subpathways of nucleotide excision repair, global genome repair, and transcription-coupled repair are not required for somatic hypermutation. This appears also to be true for mismatch repair, RAD54-dependent double-strand- break repair, and AAG-mediated base excision repair.
KW - DNA repair
KW - DNA repair-deficient mice
KW - Memory B cells
KW - Naive B cells
KW - Somatic mutations
UR - https://www.scopus.com/pages/publications/0032101017
U2 - 10.1084/jem.187.11.1735
DO - 10.1084/jem.187.11.1735
M3 - Article
C2 - 9607915
AN - SCOPUS:0032101017
SN - 0022-1007
VL - 187
SP - 1735
EP - 1742
JO - Journal of Experimental Medicine
JF - Journal of Experimental Medicine
IS - 11
ER -