Sequence‐specific <scp>DNA</scp> binding by <scp>AT</scp>‐hook motifs in Me<scp>CP</scp>2
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- Matthew J. Lyst
- The Wellcome Trust Centre for Cell Biology University of Edinburgh Edinburgh UK
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- John Connelly
- The Wellcome Trust Centre for Cell Biology University of Edinburgh Edinburgh UK
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- Cara Merusi
- The Wellcome Trust Centre for Cell Biology University of Edinburgh Edinburgh UK
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- Adrian Bird
- The Wellcome Trust Centre for Cell Biology University of Edinburgh Edinburgh UK
説明
<jats:p>Me<jats:styled-content style="fixed-case">CP</jats:styled-content>2 is a chromatin‐associated protein that is mutated in Rett syndrome. Its methyl‐CpG‐binding domain interacts with <jats:styled-content style="fixed-case">DNA</jats:styled-content> containing methylated cytosine, but other modes of recruitment to the genome have also been proposed. Here, we use <jats:italic>in vitro</jats:italic> and <jats:italic>in vivo</jats:italic> assays to investigate the <jats:styled-content style="fixed-case">DNA</jats:styled-content> binding specificity of two <jats:styled-content style="fixed-case">AT</jats:styled-content>‐hook motifs in Me<jats:styled-content style="fixed-case">CP</jats:styled-content>2. One exhibits robust sequence‐specific <jats:styled-content style="fixed-case">DNA</jats:styled-content> binding, whereas the other is a much weaker <jats:styled-content style="fixed-case">AT</jats:styled-content>‐hook. Our data indicate that these motifs are secondary contributors to <jats:styled-content style="fixed-case">DNA</jats:styled-content> binding by Me<jats:styled-content style="fixed-case">CP</jats:styled-content>2, and this view is supported by the absence of disease‐causing missense mutations at these sites.</jats:p>
収録刊行物
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- FEBS Letters
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FEBS Letters 590 (17), 2927-2933, 2016-08-09
Wiley
