Hypothesis: Biological role for J-C intronic matrix attachment regions in the molecular mechanism of antigen-driven somatic hypermutation

Andrew Franklin; Robert V. Blanden

doi:10.1111/j.1440-1711.2005.01327.x

Hypothesis: Biological role for J-C intronic matrix attachment regions in the molecular mechanism of antigen-driven somatic hypermutation

Andrew Franklin^*, Robert V. Blanden

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

3 Citations (Scopus)

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.

Original language	English
Pages (from-to)	383-391
Number of pages	9
Journal	Immunology and Cell Biology
Volume	83
Issue number	4
DOIs	https://doi.org/10.1111/j.1440-1711.2005.01327.x
Publication status	Published - Aug 2005

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title = "Hypothesis: Biological role for J-C intronic matrix attachment regions in the molecular mechanism of antigen-driven somatic hypermutation",

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.",

keywords = "Affinity maturation, Class switch recombination, DNA remodelling, Matrix attachment region, Somatic hypermutation",

author = "Andrew Franklin and Blanden, {Robert V.}",

year = "2005",

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language = "English",

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journal = "Immunology and Cell Biology",

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AU - Franklin, Andrew

AU - Blanden, Robert V.

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N2 - 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.

AB - 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.

KW - Affinity maturation

KW - Class switch recombination

KW - DNA remodelling

KW - Matrix attachment region

KW - Somatic hypermutation

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DO - 10.1111/j.1440-1711.2005.01327.x

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SP - 383

EP - 391

JO - Immunology and Cell Biology

JF - Immunology and Cell Biology

IS - 4

ER -

Hypothesis: Biological role for J-C intronic matrix attachment regions in the molecular mechanism of antigen-driven somatic hypermutation

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