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Article: The strand bias paradox of somatic hypermutation at immunoglobulin loci.

Franklin, Andrew / Blanden, Robert V

2008 Volume 29, Issue 4, Page(s) 167–172

Abstract: ... induced by the detection of uracil lesions in DNA. It is not known how, at V(D)J genes in mice ...

Abstract	Somatic hypermutation has two phases: phase 1 affects cytosine-guanine (C/G) pairs and is triggered by the deamination of cytosine residues in DNA to uracil; phase 2 affects mostly adenine-thymine (A/T) pairs and is induced by the detection of uracil lesions in DNA. It is not known how, at V(D)J genes in mice, hypermutations accumulate at A/T pairs with strand bias without perturbing the strand unbiased accumulation of hypermutations at C/G pairs. Additionally, it is not known why, in contrast, at switch regions in mice, both C/G-targeted and A/T-targeted hypermutations accumulate in a strand unbiased manner. To explain the strand bias paradox, we propose that phase 1 and phase 2 hypermutations are generated at different stages of the cell cycle.
MeSH term(s)	Animals ; Antibody Diversity/genetics ; Antibody Diversity/immunology ; Base Pairing ; Cell Cycle/genetics ; Gene Rearrangement, B-Lymphocyte ; Genes, Immunoglobulin ; Humans ; Immunoglobulins/genetics ; Immunoglobulins/immunology ; Mutagenesis ; Somatic Hypermutation, Immunoglobulin
Chemical Substances	Immunoglobulins
Language	English
Publishing date	2008-04
Publishing country	England
Document type	Journal Article
ZDB-ID	2036831-8
ISSN	1471-4981 ; 1471-4906
ISSN (online)	1471-4981
ISSN	1471-4906
DOI	10.1016/j.it.2008.01.008
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Article: A/T-targeted somatic hypermutation: critique of the mainstream model.

Franklin, Andrew / Blanden, Robert V

Trends in biochemical sciences

2006 Volume 31, Issue 5, Page(s) 252–258

Abstract: The "affinity maturation" of the humoral immune response is driven by antigen-activated somatic hypermutation (SHM) of the genes that encode antibody variable regions and the subsequent antigenic selection of mutant clones. The molecular mechanism of SHM ...

Abstract	The "affinity maturation" of the humoral immune response is driven by antigen-activated somatic hypermutation (SHM) of the genes that encode antibody variable regions and the subsequent antigenic selection of mutant clones. The molecular mechanism of SHM is yet to be completely elucidated. SHM affects cytosine-guanine (C/G) and adenine-thymine (A/T) pairs with approximately equal frequency in vivo. The proposition that error-prone DNA-dependent DNA synthesis explains A/T-targeted hypermutagenesis seems to have mainstream support within the hypermutation research community at present. A major feature of SHM in vivo is that C/G hypermutation is strand unbiased, whereas A/T hypermutation is strand biased. We show that the "DNA-based polymerase error" model of A/T-targeted hypermutagenesis does not explain this important aspect of SHM.
MeSH term(s)	Adenine/chemistry ; Animals ; Base Pairing ; Gene Targeting ; Humans ; Immunoglobulin Variable Region/genetics ; Models, Genetic ; Somatic Hypermutation, Immunoglobulin/genetics ; Thymine/chemistry
Chemical Substances	Immunoglobulin Variable Region ; Adenine (JAC85A2161) ; Thymine (QR26YLT7LT)
Language	English
Publishing date	2006-05
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	194216-5
ISSN	1362-4326 ; 0968-0004 ; 0376-5067
ISSN (online)	1362-4326
ISSN	0968-0004 ; 0376-5067
DOI	10.1016/j.tibs.2006.03.008
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Article: Potential inhibition of somatic hypermutation by nucleoside analogues.

Franklin, Andrew / Blanden, Robert V

Molecular immunology

2006 Volume 44, Issue 4, Page(s) 666–669

Abstract: Somatic hypermutation, which occurs in antigen-activated germinal centre B lymphocytes, diversifies the genes that encode immunoglobulin variable regions and leads to the 'affinity maturation' of the humoral immune response. Hypermutation affects dC/dG ... ...

Abstract	Somatic hypermutation, which occurs in antigen-activated germinal centre B lymphocytes, diversifies the genes that encode immunoglobulin variable regions and leads to the 'affinity maturation' of the humoral immune response. Hypermutation affects dC/dG and dA/dT pairs with approximately equal frequency in vivo. DNA polymerase-theta contributes to hypermutagenesis at dC/dG pairs and DNA polymerase-eta is substantially involved in the generation of hypermutations at dA/dT pairs. The biochemical properties of polymerases-theta and -eta indicate that their DNA synthetic activities are potentially susceptible to inhibition by nucleoside analogues, so it is feasible that nucleoside analogues reduce the accumulation of dC/dG- and dA/dT-targeted hypermutations in vivo. Nucleoside analogues could hence impair the humoral adaptive immune response of HIV-infected patients who are prescribed these chemotherapeutic agents.
MeSH term(s)	B-Lymphocytes/immunology ; DNA Replication/immunology ; DNA-Directed DNA Polymerase/genetics ; DNA-Directed DNA Polymerase/immunology ; HIV Infections/genetics ; HIV Infections/immunology ; HIV-1/genetics ; HIV-1/immunology ; Humans ; Nucleosides/genetics ; Nucleosides/immunology ; Nucleosides/pharmacology ; Somatic Hypermutation, Immunoglobulin/drug effects ; DNA Polymerase theta
Chemical Substances	Nucleosides ; DNA-Directed DNA Polymerase (EC 2.7.7.7)
Language	English
Publishing date	2006-04-03
Publishing country	England
Document type	Journal Article
ZDB-ID	424427-8
ISSN	1872-9142 ; 0161-5890
ISSN (online)	1872-9142
ISSN	0161-5890
DOI	10.1016/j.molimm.2006.02.022
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Article: Hypothesis: biological role for J-C intronic matrix attachment regions in the molecular mechanism of antigen-driven somatic hypermutation.

Franklin, Andrew / Blanden, Robert V

Immunology and cell biology

2005 Volume 83, Issue 4, Page(s) 383–391

Abstract: 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 ... ...

Abstract	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.
MeSH term(s)	Antigens/immunology ; B-Lymphocytes/immunology ; B-Lymphocytes/metabolism ; Gene Rearrangement, B-Lymphocyte/genetics ; Introns/genetics ; Matrix Attachment Regions/genetics ; Models, Genetic ; Models, Immunological ; Nucleic Acid Conformation ; Somatic Hypermutation, Immunoglobulin/genetics ; Somatic Hypermutation, Immunoglobulin/immunology
Chemical Substances	Antigens
Language	English
Publishing date	2005-08
Publishing country	United States
Document type	Journal Article
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1111/j.1440-1711.2005.01327.x
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Article: On the molecular mechanism of somatic hypermutation of rearranged immunoglobulin genes.

Franklin, Andrew / Blanden, Robert V

Immunology and cell biology

2004 Volume 82, Issue 6, Page(s) 557–567

Abstract: Somatic hypermutation (SHM) diversifies the genes that encode immunoglobulin variable regions in antigen-activated germinal centre B lymphocytes. Available evidence strongly suggests that DNA deamination potentiates phase I SHM and subsequently triggers ... ...

Abstract	Somatic hypermutation (SHM) diversifies the genes that encode immunoglobulin variable regions in antigen-activated germinal centre B lymphocytes. Available evidence strongly suggests that DNA deamination potentiates phase I SHM and subsequently triggers phase II SHM. A concise review of this evidence is followed by a detailed critique of two possible models which suggest that polymerase-eta potentiates phase II SHM via either its DNA-dependent or its RNA-dependent DNA synthetic activity. Quantitative analysis, in the context of extant data that define the features of SHM, favours the RNA-dependent mechanism.
MeSH term(s)	Animals ; Gene Rearrangement/genetics ; Genes, Immunoglobulin/genetics ; Humans ; Models, Genetic ; Somatic Hypermutation, Immunoglobulin/genetics
Language	English
Publishing date	2004-12
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1111/j.1440-1711.2004.01289.x
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Article: Genesis of the strand-biased signature in somatic hypermutation of rearranged immunoglobulin variable genes.

Steele, Edward J / Franklin, Andrew / Blanden, Robert V

Immunology and cell biology

2004 Volume 82, Issue 2, Page(s) 209–218

Abstract: ... in rearranged immunoglobulin variable genes (V(D)J). The recent disagreement in the field as to whether strand ... presence, in some mutated V(D)J sequence collections, of polymerase chain reaction (PCR)-recombinant ... in all mouse and human collections of somatically mutated V(D)J sequences. This evidence, together with our own ...

Abstract	The history and current development of the reverse transcriptase model of somatic hypermutation (RT-model) is reviewed with particular reference to the genesis of strand-biased mutation signatures in rearranged immunoglobulin variable genes (V(D)J). The recent disagreement in the field as to whether strand bias really exists or not has been critically analysed and the confusion traced to the putative presence, in some mutated V(D)J sequence collections, of polymerase chain reaction (PCR)-recombinant artefacts. Recent analysis of somatic hypermutation in xeroderma pigmentosum variant patients, by the group of PJ Gearhart and others, has established that the Y-family translesion DNA repair enzyme, DNA polymerase eta (eta), is responsible for the striking A-T targeted strand-bias mutation signature seen in all mouse and human collections of somatically mutated V(D)J sequences. This evidence, together with our own recent demonstration that human DNA polymerase eta is a reverse transcriptase, leads to the conclusion that the strand-biased A-T mutation signature is caused either by: (i) error-prone DNA-dependent DNA repair synthesis by pol-eta of single-strand nicks preferentially in the non-transcribed strand; and/or (ii) by error-prone cDNA synthesis of the transcribed strand by pol-eta using the pre-mRNA as the copying template, primed by the nicked transcribed DNA strand, followed by replacement of the original transcribed strand by cDNA. Analysis of the total mutation pattern also suggests that the major transitions observed in SHM (A-->G, C-->T and G-->A) can be explained by known RNA editing mechanisms active on pre-mRNA which are then written into cDNA during synthesis of the transcribed strand by error-prone cellular reverse transcriptases such as pol-eta.
MeSH term(s)	Animals ; DNA-Directed DNA Polymerase/genetics ; DNA-Directed DNA Polymerase/metabolism ; Gene Rearrangement ; Humans ; Immunoglobulin Variable Region/genetics ; Immunoglobulin Variable Region/metabolism ; Mutation ; Polymerase Chain Reaction ; RNA Editing/physiology ; RNA-Directed DNA Polymerase/metabolism ; Xeroderma Pigmentosum/enzymology ; Xeroderma Pigmentosum/genetics
Chemical Substances	Immunoglobulin Variable Region ; RNA-Directed DNA Polymerase (EC 2.7.7.49) ; DNA-Directed DNA Polymerase (EC 2.7.7.7) ; Rad30 protein (EC 2.7.7.7)
Language	English
Publishing date	2004-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1046/j.0818-9641.2004.01224.x
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Article: The boundaries of the distribution of somatic hypermutation of rearranged immunoglobulin variable genes.

Blanden, Robert V / Franklin, Andrew / Steele, Edward J

Immunology and cell biology

2004 Volume 82, Issue 2, Page(s) 205–208

Abstract: Available evidence about the mechanisms and distribution of somatic hypermutation (SHM) of rearranged immunoglobulin (IgV) genes is reviewed with particular emphasis on the 5' boundary. In heavy (H) chain genes, the 5' boundary of SHM is the ... ...

Abstract	Available evidence about the mechanisms and distribution of somatic hypermutation (SHM) of rearranged immunoglobulin (IgV) genes is reviewed with particular emphasis on the 5' boundary. In heavy (H) chain genes, the 5' boundary of SHM is the transcription start site; in contrast to kappa light (L) chain genes, it is located in the leader (L) intron. DNA-based models of SHM cannot account for this difference. However, an updated reverse transcriptase (RT)-based model invoking error-prone RT activity of DNA polymerase eta copying IgV pre-mRNA templates to produce cDNA of the transcribed strand (TS) of IgV DNA, which then replaces the corresponding section of the original TS, can explain the difference. This explanation incorporates recent knowledge of pre-mRNA processing, in particular, binding of the splicing-associated protein termed U2AF to a pyrimidine-rich tract in the L intron of pre-mRNA of kappa L chains that may block RT progression further upstream to the end of the pre-mRNA template (transcription start site). Reasons why this block may not occur in H chains and other aspects of the updated RT-model are discussed.
MeSH term(s)	Animals ; Gene Rearrangement ; Humans ; Immunoglobulin Variable Region/genetics ; Mutation
Chemical Substances	Immunoglobulin Variable Region
Language	English
Publishing date	2004-04
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1046/j.0818-9641.2004.01226.x
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Article: Human DNA polymerase-eta, an A-T mutator in somatic hypermutation of rearranged immunoglobulin genes, is a reverse transcriptase.

Franklin, Andrew / Milburn, Peter J / Blanden, Robert V / Steele, Edward J

Immunology and cell biology

2004 Volume 82, Issue 2, Page(s) 219–225

Abstract: We have proposed previously that error-prone reverse transcription using pre-mRNA of rearranged immunoglobulin variable (IgV) regions as templates is involved in the antibody diversifying mechanism of somatic hypermutation (SHM). As patients deficient in ...

Abstract	We have proposed previously that error-prone reverse transcription using pre-mRNA of rearranged immunoglobulin variable (IgV) regions as templates is involved in the antibody diversifying mechanism of somatic hypermutation (SHM). As patients deficient in DNA polymerase-eta exhibit an abnormal spectrum of SHM, we postulated that this recently discovered Y-family polymerase is a reverse transcriptase (RT). This possibility was tested using a product-enhanced RT (PERT) assay that uses a real time PCR step with a fluorescent probe to detect cDNA products of at least 27-37 nucleotides. Human pol-eta and two other Y-family enzymes that are dispensable for SHM, human pols-iota and -kappa, copied a heteropolymeric DNA-primed RNA template in vitro under conditions with substantial excesses of template. Repeated experiments gave highly reproducible results. The RT activity detected using one aliquot of human pol-eta was confirmed using a second sample from an independent source. Human DNA pols-beta and -mu, and T4 DNA polymerase repeatedly demonstrated no RT activity. Pol-eta was the most efficient RT of the Y-family enzymes assayed but was much less efficient than an HIV-RT standard in vitro. It is thus feasible that pol-eta acts as both a RNA- and a DNA-dependent DNA polymerase in SHM in vivo, and that Y-family RT activity participates in other mechanisms of physiological importance.
MeSH term(s)	Base Sequence ; DNA-Directed DNA Polymerase/genetics ; DNA-Directed DNA Polymerase/metabolism ; Gene Rearrangement ; Humans ; Immunoglobulin Variable Region/genetics ; Immunoglobulin Variable Region/metabolism ; Molecular Sequence Data ; Mutation ; RNA-Directed DNA Polymerase/metabolism
Chemical Substances	Immunoglobulin Variable Region ; DNA polymerase iota (EC 2.7.7.-) ; RNA-Directed DNA Polymerase (EC 2.7.7.49) ; DNA-Directed DNA Polymerase (EC 2.7.7.7) ; POLK protein, human (EC 2.7.7.7) ; Rad30 protein (EC 2.7.7.7)
Language	English
Publishing date	2004-04
Publishing country	United States
Document type	Journal Article
ZDB-ID	284057-1
ISSN	1440-1711 ; 0818-9641
ISSN (online)	1440-1711
ISSN	0818-9641
DOI	10.1046/j.0818-9641.2004.01221.x
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Article: Molecular evolution of V(H)9 germline genes isolated from DBA, BALB, 129 and C57BL mouse strains and sublines.

Zylstra, Paula / Franklin, Andrew / Hassan, Karl A / Powell, Kim L / Steele, Edward J / Blanden, Robert V

Immunogenetics

2003 Volume 55, Issue 3, Page(s) 182–188

Abstract: ... hitherto unavailable contiguous flanks of all members of the small V(H) 9 germline gene family ... evolution of these sequences. Fifteen genuine germline genes were isolated (designated V(H) 9.1 through V(H ... nine are novel: seven sequences from DBA strains and sublines ( V(H) 9.3 to V(H) 9.9) and two sequences ...

Abstract	We have used the polymerase chain reaction (PCR) in an attempt to clone and sequence the exons and hitherto unavailable contiguous flanks of all members of the small V(H) 9 germline gene family from inbred mouse strains and sublines that have had a common ancestry within the last century, and to analyze the molecular evolution of these sequences. Fifteen genuine germline genes were isolated (designated V(H) 9.1 through V(H) 9.15) from strains and sublines of DBA, BALB, 129 and C57BL inbred mice. Of the 15 genuine isolates, nine are novel: seven sequences from DBA strains and sublines ( V(H) 9.3 to V(H) 9.9) and two sequences from C57BL strains ( V(H) 9.13 and V(H) 9.14). We have identified sequencing errors and PCR recombinant artefacts in previously published sequences. We detected no sequence divergence of individual genes shared by the strains and sublines studied. However, we isolated two genes from DBA strains and sublines, V(H) 9.1 and V(H) 9.3, that differ only by five nucleotides encoding three amino acid changes that are concentrated within a 33 nucleotide (11 codon) region. Of these 11 codons, eight encode a putative antigen binding site. There were no differences in the remaining 733 nucleotides sequenced (including both 5' and 3' flanking regions). Potential explanations for the generation of V(H) 9.1 and V(H) 9.3 are discussed.
MeSH term(s)	Animals ; Base Sequence ; Evolution, Molecular ; Immunoglobulin Variable Region/genetics ; Mice ; Mice, Inbred BALB C/genetics ; Mice, Inbred C57BL/genetics ; Mice, Inbred DBA/genetics ; Molecular Sequence Data ; Phylogeny ; Sequence Alignment
Chemical Substances	Immunoglobulin Variable Region
Language	English
Publishing date	2003-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	186560-2
ISSN	1432-1211 ; 0093-7711
ISSN (online)	1432-1211
ISSN	0093-7711
DOI	10.1007/s00251-003-0565-x
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Article: Lack of both Fas ligand and perforin protects from flavivirus-mediated encephalitis in mice.

Licon Luna, Rosa M / Lee, Eva / Müllbacher, Arno / Blanden, Robert V / Langman, Rod / Lobigs, Mario

Journal of virology

2001 Volume 76, Issue 7, Page(s) 3202–3211

Abstract: The mechanism by which encephalitic flaviviruses enter the brain to inflict a life-threatening encephalomyelitis in a small percentage of infected individuals is obscure. We investigated this issue in a mouse model for flavivirus encephalitis in which ... ...

Abstract	The mechanism by which encephalitic flaviviruses enter the brain to inflict a life-threatening encephalomyelitis in a small percentage of infected individuals is obscure. We investigated this issue in a mouse model for flavivirus encephalitis in which the virus was administered to 6-week-old animals by the intravenous route, analogous to the portal of entry in natural infections, using a virus dose in the range experienced following the bite of an infectious mosquito. In this model, infection with 0.1 to 10(5) PFU of virus gave mortality in approximately 50% of animals despite low or undetectable virus growth in extraneural tissues. We show that the cytolytic effector functions play a crucial role in invasion of the encephalitic flavivirus into the brain. Mice deficient in either the granule exocytosis- or Fas-mediated pathway of cytotoxicity showed delayed and reduced mortality. Mice deficient in both cytotoxic effector functions were resistant to a low-dose peripheral infection with the neurotropic virus.
MeSH term(s)	Animals ; Brain/virology ; Cell Line ; Disease Models, Animal ; Encephalitis Virus, Murray Valley ; Encephalitis, Arbovirus/immunology ; Encephalitis, Arbovirus/virology ; Fas Ligand Protein ; Flaviviridae Infections/immunology ; Flaviviridae Infections/virology ; Membrane Glycoproteins/deficiency ; Membrane Glycoproteins/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Perforin ; Pore Forming Cytotoxic Proteins ; T-Lymphocytes, Cytotoxic/immunology ; fas Receptor/genetics ; fas Receptor/physiology
Chemical Substances	Fas Ligand Protein ; Fasl protein, mouse ; Membrane Glycoproteins ; Pore Forming Cytotoxic Proteins ; fas Receptor ; Perforin (126465-35-8)
Language	English
Publishing date	2001-05-07
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/jvi.76.7.3202-3211.2002
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