Mechanisms of tandem repeat instability in bacteria
作者： M. Bichara , J. Wagner , I.B. Lambert
DOI: 10.1016/J.MRFMMM.2006.01.020
关键词: DNA 、 Base pair 、 Genetics 、 DNA repair 、 DNA Repeat Expansion 、 Gene 、 Genome 、 Biology 、 Genome instability 、 Tandem repeat 、 Health, Toxicology and Mutagenesis 、 Molecular biology
摘要: Hypermutable tandem repeat sequences (TRSs) are present in the genomes of both prokaryotic and eukaryotic organisms. Numerous studies have been conducted several laboratories over past decade to investigate mechanisms responsible for expansions contractions microsatellites (a subset TRSs with a length 1-6 nucleotides) model organism Escherichia coli. Both frequency instability (TRI), types mutational events that arise, markedly influenced by DNA sequence repeat, number unit repeats, cellular pathways process TRS. strand slippage is general mechanism invoked explain TRSs. Misaligned stabilized favorable base pairing complementary propensity form relatively stable secondary structures. Several processes, including replication, recombination variety repair pathways, shown interact such structures influence TRI bacteria. This paper provides an overview our current understanding bacteria, emphasis on carried out E. In addition, new experimental data presented, suggesting TLS polymerases (PolII, PolIV PolV) do not contribute significantly
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