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dc.contributor.author
Campo, Vanina A.
dc.contributor.author
Patenaude, Anne-Marie
dc.contributor.author
Kaden, Svenja
dc.contributor.author
Horb, Lori
dc.contributor.author
Firka, Daniel
dc.contributor.author
Jiricny, Josef
dc.contributor.author
Di Noia, Javier M.
dc.date.accessioned
2019-04-02T15:43:36Z
dc.date.available
2017-06-10T16:20:47Z
dc.date.available
2019-04-02T15:43:36Z
dc.date.issued
2013-03
dc.identifier.issn
1362-4962
dc.identifier.issn
0305-1048
dc.identifier.issn
1362-4954
dc.identifier.other
10.1093/nar/gks1470
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/66142
dc.identifier.doi
10.3929/ethz-b-000066142
dc.description.abstract
The mammalian antibody repertoire is shaped by somatic hypermutation (SHM) and class switch recombination (CSR) of the immunoglobulin ( Ig ) loci of B lymphocytes. SHM and CSR are triggered by non-canonical, error-prone processing of G/U mismatches generated by activation-induced deaminase (AID). In birds, AID does not trigger SHM, but it triggers Ig gene conversion (GC), a ‘homeologous’ recombination process involving the Ig variable region and proximal pseudogenes. Because recombination fidelity is controlled by the mismatch repair (MMR) system, we investigated whether MMR affects GC in the chicken B cell line DT40. We show here that Msh6 −/− and Pms2 −/− DT40 cells display cell cycle defects, including genomic re-replication. However, although IgVλ GC tracts in MMR-deficient cells were slightly longer than in normal cells, Ig GC frequency, donor choice or the number of mutations per sequence remained unaltered. The finding that the avian MMR system, unlike that of mammals, does not seem to contribute towards the processing of G/U mismatches in vitro could explain why MMR is unable to initiate Ig GC in this species, despite initiating SHM and CSR in mammalian cells. Moreover, as MMR does not counteract or govern Ig GC, we report a rare example of ‘homeologous’ recombination insensitive to MMR.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Oxford University Press
en_US
dc.rights.uri
http://creativecommons.org/licenses/by-nc/3.0/
dc.title
MSH6- or PMS2-deficiency causes re-replication in DT40 B cells, but it has little effect on immunoglobulin gene conversion or on repair of AID-generated uracils
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution-NonCommercial 3.0 Unported
dc.date.published
2013-01-10
ethz.journal.title
Nucleic Acids Research
ethz.journal.volume
41
en_US
ethz.journal.issue
5
en_US
ethz.journal.abbreviated
Nucleic Acids Res.
ethz.pages.start
3032
en_US
ethz.pages.end
3046
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.nebis
000038633
ethz.publication.place
Oxford
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::03667 - Jiricny, Josef (emeritus)
en_US
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02030 - Dep. Biologie / Dep. of Biology::03667 - Jiricny, Josef (emeritus)
ethz.date.deposited
2017-06-10T16:21:20Z
ethz.source
ECIT
ethz.identifier.importid
imp5936508a9350815099
ethz.ecitpid
pub:105479
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2017-07-14T14:36:20Z
ethz.rosetta.lastUpdated
2019-04-02T15:44:13Z
ethz.rosetta.versionExported
true
ethz.COinS
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