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Enhanced CpG Mutability and Tumorigenesis in MBD4-Deficient Mice

Millar, Catherine B., Guy, Jacky, Sansom, Owen J., Selfridge, Jim, MacDougall, Eilidh, Hendrich, Brian, Keightley,, Peter D., Bishop, Stefan Mark, Clarke, Alan Richard and Bird, Adrian 2002. Enhanced CpG Mutability and Tumorigenesis in MBD4-Deficient Mice. Science , pp. 403-405. 10.1126/science.1073354

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The mammalian protein MBD4 contains a methyl-CpG binding domain and can enzymatically remove thymine (T) or uracil (U) from a mismatched CpG site in vitro. These properties suggest that MBD4 might function in vivo to minimize the mutability of 5-methylcytosine by removing its deamination product from DNA. We tested this hypothesis by analyzing Mbd4/ mice and found that the frequency of of C T transitions at CpG sites was increased by a factor of three. On a cancer-susceptible ApcMin/+ background, Mbd4/ mice showed accelerated tumor formation with CpG TpG mutations in the Apc gene. Thus MBD4 suppresses CpG mutability and tumorigenesis in vivo.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Biosciences
ISSN: 1095-9203
Last Modified: 01 Feb 2020 23:14

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