The Fanconi anemia core complex is dispensable during somatic hypermutation and class switch recombination.
To generate high affinity antibodies during an immune response, B cells undergo somatic hypermutation (SHM) of their immunoglobulin genes. Error-prone translesion synthesis (TLS) DNA polymerases have been reported to be responsible for all mutations at template A/T and at least a fraction of G/C tra...
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doaj-d2e77dad11a5417ab2ff7bdcb316ff152020-11-25T02:15:31ZengPublic Library of Science (PLoS)PLoS ONE1932-62032010-01-01512e1523610.1371/journal.pone.0015236The Fanconi anemia core complex is dispensable during somatic hypermutation and class switch recombination.Peter H L KrijgerNiek WitPaul C M van den BerkHeinz JacobsTo generate high affinity antibodies during an immune response, B cells undergo somatic hypermutation (SHM) of their immunoglobulin genes. Error-prone translesion synthesis (TLS) DNA polymerases have been reported to be responsible for all mutations at template A/T and at least a fraction of G/C transversions. In contrast to A/T mutations which depend on PCNA ubiquitination, it remains unclear how G/C transversions are regulated during SHM. Several lines of evidence indicate a mechanistic link between the Fanconi Anemia (FA) pathway and TLS. To investigate the contribution of the FA pathway in SHM we analyzed FancG-deficient B cells. B cells deficient for FancG, an essential member of the FA core complex, were hypersensitive to treatment with cross-linking agents. However, the frequencies and nucleotide exchange spectra of SHM remained comparable between wild-type and FancG-deficient B cells. These data indicate that the FA pathway is not involved in regulating the outcome of SHM in mammals. In addition, the FA pathway appears dispensable for class switch recombination.http://europepmc.org/articles/PMC3012132?pdf=render |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Peter H L Krijger Niek Wit Paul C M van den Berk Heinz Jacobs |
spellingShingle |
Peter H L Krijger Niek Wit Paul C M van den Berk Heinz Jacobs The Fanconi anemia core complex is dispensable during somatic hypermutation and class switch recombination. PLoS ONE |
author_facet |
Peter H L Krijger Niek Wit Paul C M van den Berk Heinz Jacobs |
author_sort |
Peter H L Krijger |
title |
The Fanconi anemia core complex is dispensable during somatic hypermutation and class switch recombination. |
title_short |
The Fanconi anemia core complex is dispensable during somatic hypermutation and class switch recombination. |
title_full |
The Fanconi anemia core complex is dispensable during somatic hypermutation and class switch recombination. |
title_fullStr |
The Fanconi anemia core complex is dispensable during somatic hypermutation and class switch recombination. |
title_full_unstemmed |
The Fanconi anemia core complex is dispensable during somatic hypermutation and class switch recombination. |
title_sort |
fanconi anemia core complex is dispensable during somatic hypermutation and class switch recombination. |
publisher |
Public Library of Science (PLoS) |
series |
PLoS ONE |
issn |
1932-6203 |
publishDate |
2010-01-01 |
description |
To generate high affinity antibodies during an immune response, B cells undergo somatic hypermutation (SHM) of their immunoglobulin genes. Error-prone translesion synthesis (TLS) DNA polymerases have been reported to be responsible for all mutations at template A/T and at least a fraction of G/C transversions. In contrast to A/T mutations which depend on PCNA ubiquitination, it remains unclear how G/C transversions are regulated during SHM. Several lines of evidence indicate a mechanistic link between the Fanconi Anemia (FA) pathway and TLS. To investigate the contribution of the FA pathway in SHM we analyzed FancG-deficient B cells. B cells deficient for FancG, an essential member of the FA core complex, were hypersensitive to treatment with cross-linking agents. However, the frequencies and nucleotide exchange spectra of SHM remained comparable between wild-type and FancG-deficient B cells. These data indicate that the FA pathway is not involved in regulating the outcome of SHM in mammals. In addition, the FA pathway appears dispensable for class switch recombination. |
url |
http://europepmc.org/articles/PMC3012132?pdf=render |
work_keys_str_mv |
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