| pubmed-article:10359804 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10359804 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:10359804 | lifeskim:mentions | umls-concept:C0014834 | lld:lifeskim |
| pubmed-article:10359804 | lifeskim:mentions | umls-concept:C0026882 | lld:lifeskim |
| pubmed-article:10359804 | lifeskim:mentions | umls-concept:C0205374 | lld:lifeskim |
| pubmed-article:10359804 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:10359804 | pubmed:dateCreated | 1999-7-8 | lld:pubmed |
| pubmed-article:10359804 | pubmed:abstractText | Microbial populations under nonlethal selection can give rise to mutations that relieve the selective pressure, a phenomenon that has come to be called "adaptive mutation." One explanation for adaptive mutation is that a small proportion of the cells experience a period of transient hypermutation, and that these hypermutators account for the mutations that appear. The experiments reported here investigated the contribution that hypermutators make to the mutations occurring in a Lac- strain of Escherichia coli during selection for lactose utilization. A broad mutational screen, loss of motility, was used to compare the frequency of nonselected mutations in starved Lac- cells, in Lac+ revertants, and in Lac+ revertants carrying yet another nonselected mutation. These frequencies allowed us to calculate that the hypermutating subpopulation makes up approximately 0.06% of the population and that its mutation rate is elevated approximately 200-fold. From these numbers we conclude that the hypermutators are responsible for nearly all multiple mutations but produce only approximately 10% of the adaptive Lac+ mutations. | lld:pubmed |
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| pubmed-article:10359804 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10359804 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10359804 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:10359804 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10359804 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:10359804 | pubmed:issn | 0027-8424 | lld:pubmed |
| pubmed-article:10359804 | pubmed:author | pubmed-author:FosterP LPL | lld:pubmed |
| pubmed-article:10359804 | pubmed:author | pubmed-author:RoscheW AWA | lld:pubmed |
| pubmed-article:10359804 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10359804 | pubmed:day | 8 | lld:pubmed |
| pubmed-article:10359804 | pubmed:volume | 96 | lld:pubmed |
| pubmed-article:10359804 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10359804 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10359804 | pubmed:pagination | 6862-7 | lld:pubmed |
| pubmed-article:10359804 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
| pubmed-article:10359804 | pubmed:meshHeading | pubmed-meshheading:10359804... | lld:pubmed |
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| pubmed-article:10359804 | pubmed:meshHeading | pubmed-meshheading:10359804... | lld:pubmed |
| pubmed-article:10359804 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10359804 | pubmed:articleTitle | The role of transient hypermutators in adaptive mutation in Escherichia coli. | lld:pubmed |
| pubmed-article:10359804 | pubmed:affiliation | Department of Environmental Health, Boston University School of Public Health, Boston University School of Medicine, Boston, MA 02118, USA. | lld:pubmed |
| pubmed-article:10359804 | pubmed:publicationType | Journal Article | lld:pubmed |
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