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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America. >Strand-biased cytosine deamination at the replication fork causes cytosine to thymine mutations in Escherichia coli
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Strand-biased cytosine deamination at the replication fork causes cytosine to thymine mutations in Escherichia coli

机译：Strand-biased cytosine deamination at the replication fork causes cytosine to thymine mutations in Escherichia coli

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摘要

The rate of cytosine deamination is much higher in single-stranded DNA (ssDNA) than in double-stranded DNA, and copying the resulting uracils causes C to T mutations. To study this phenomenon, the catalytic domain of APOBEC3G (A3G-CTD), an ssDNA-specific cytosine deaminase, was expressed in an Escherichia coli strain defective in uracil repair (ung mutant), and the mutations that accumulated over thousands of generations were determined by whole-genome sequencing. C: G to T: A transitions dominated, with significantly more cytosines mutated to thymine in the lagging-strand template (LGST) than in the leading-strand template (LDST). This strand bias was present in both repair-defective and repair-proficient cells and was strongest and highly significant in cells expressing A3G-CTD. These results show that the LGST is accessible to cellular cytosine deaminating agents, explains the well-known GC skew in microbial genomes, and suggests the APOBEC3 family of mutators may target the LGST in the human genome.

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