| pubmed-article:21673140 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:21673140 | lifeskim:mentions | umls-concept:C0524637 | lld:lifeskim |
| pubmed-article:21673140 | lifeskim:mentions | umls-concept:C0012854 | lld:lifeskim |
| pubmed-article:21673140 | lifeskim:mentions | umls-concept:C0033684 | lld:lifeskim |
| pubmed-article:21673140 | lifeskim:mentions | umls-concept:C0678594 | lld:lifeskim |
| pubmed-article:21673140 | lifeskim:mentions | umls-concept:C0445356 | lld:lifeskim |
| pubmed-article:21673140 | lifeskim:mentions | umls-concept:C1527178 | lld:lifeskim |
| pubmed-article:21673140 | pubmed:issue | 26 | lld:pubmed |
| pubmed-article:21673140 | pubmed:dateCreated | 2011-6-29 | lld:pubmed |
| pubmed-article:21673140 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21673140 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21673140 | pubmed:abstractText | H-NS and Lsr2 are nucleoid-associated proteins from Gram-negative bacteria and Mycobacteria, respectively, that play an important role in the silencing of horizontally acquired foreign DNA that is more AT-rich than the resident genome. Despite the fact that Lsr2 and H-NS proteins are dissimilar in sequence and structure, they serve apparently similar functions and can functionally complement one another. The mechanism by which these xenogeneic silencers selectively target AT-rich DNA has been enigmatic. We performed high-resolution protein binding microarray analysis to simultaneously assess the binding preference of H-NS and Lsr2 for all possible 8-base sequences. Concurrently, we performed a detailed structure-function relationship analysis of their C-terminal DNA binding domains by NMR. Unexpectedly, we found that H-NS and Lsr2 use a common DNA binding mechanism where a short loop containing a "Q/RGR" motif selectively interacts with the DNA minor groove, where the highest affinity is for AT-rich sequences that lack A-tracts. Mutations of the Q/RGR motif abolished DNA binding activity. Netropsin, a DNA minor groove-binding molecule effectively outcompeted H-NS and Lsr2 for binding to AT-rich sequences. These results provide a unified molecular mechanism to explain findings related to xenogeneic silencing proteins, including their lack of apparent sequence specificity but preference for AT-rich sequences. Our findings also suggest that structural information contained within the DNA minor groove is deciphered by xenogeneic silencing proteins to distinguish genetic material that is self from nonself. | lld:pubmed |
| pubmed-article:21673140 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21673140 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21673140 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21673140 | pubmed:language | eng | lld:pubmed |
| pubmed-article:21673140 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21673140 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:21673140 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21673140 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21673140 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21673140 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:21673140 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:21673140 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:21673140 | pubmed:issn | 1091-6490 | lld:pubmed |
| pubmed-article:21673140 | pubmed:author | pubmed-author:LowM BMB | lld:pubmed |
| pubmed-article:21673140 | pubmed:author | pubmed-author:TyoJ SJS | lld:pubmed |
| pubmed-article:21673140 | pubmed:author | pubmed-author:HughesTimothy... | lld:pubmed |
| pubmed-article:21673140 | pubmed:author | pubmed-author:NavarreWillia... | lld:pubmed |
| pubmed-article:21673140 | pubmed:author | pubmed-author:WeirauchMatth... | lld:pubmed |
| pubmed-article:21673140 | pubmed:author | pubmed-author:LiYifeiY | lld:pubmed |
| pubmed-article:21673140 | pubmed:author | pubmed-author:GordonBlair... | lld:pubmed |
| pubmed-article:21673140 | pubmed:author | pubmed-author:CoteAtinaA | lld:pubmed |
| pubmed-article:21673140 | pubmed:author | pubmed-author:DingPengfeiP | lld:pubmed |
| pubmed-article:21673140 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:21673140 | pubmed:day | 28 | lld:pubmed |
| pubmed-article:21673140 | pubmed:volume | 108 | lld:pubmed |
| pubmed-article:21673140 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:21673140 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:21673140 | pubmed:pagination | 10690-5 | lld:pubmed |
| pubmed-article:21673140 | pubmed:meshHeading | pubmed-meshheading:21673140... | lld:pubmed |
| pubmed-article:21673140 | pubmed:meshHeading | pubmed-meshheading:21673140... | lld:pubmed |
| pubmed-article:21673140 | pubmed:meshHeading | pubmed-meshheading:21673140... | lld:pubmed |
| pubmed-article:21673140 | pubmed:meshHeading | pubmed-meshheading:21673140... | lld:pubmed |
| pubmed-article:21673140 | pubmed:meshHeading | pubmed-meshheading:21673140... | lld:pubmed |
| pubmed-article:21673140 | pubmed:meshHeading | pubmed-meshheading:21673140... | lld:pubmed |
| pubmed-article:21673140 | pubmed:meshHeading | pubmed-meshheading:21673140... | lld:pubmed |
| pubmed-article:21673140 | pubmed:meshHeading | pubmed-meshheading:21673140... | lld:pubmed |
| pubmed-article:21673140 | pubmed:meshHeading | pubmed-meshheading:21673140... | lld:pubmed |
| pubmed-article:21673140 | pubmed:meshHeading | pubmed-meshheading:21673140... | lld:pubmed |
| pubmed-article:21673140 | pubmed:meshHeading | pubmed-meshheading:21673140... | lld:pubmed |
| pubmed-article:21673140 | pubmed:year | 2011 | lld:pubmed |
| pubmed-article:21673140 | pubmed:articleTitle | Structural basis for recognition of AT-rich DNA by unrelated xenogeneic silencing proteins. | lld:pubmed |
| pubmed-article:21673140 | pubmed:affiliation | Department of Molecular Genetics, University of Toronto, Toronto, ON, Canada M5S 1A8. | lld:pubmed |
| pubmed-article:21673140 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:21673140 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
