Linked Life Data

20577816

Source:http://linkedlifedata.com/resource/pubmed/id/20577816

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2011-1-21
pubmed:abstractText
The physiological roles of the mitochondrial transcription termination factor (mTERF) family are poorly understood. MTERF and its homologues influence transcriptional readthrough in vitro, but the extent to which they regulate mitochondrial RNA levels in vivo is unclear. In addition, MTERF was previously shown to promote replication pausing. To test their roles in mtDNA metabolism, we created cell-lines inducibly expressing epitope-tagged versions of two members of the mTERF family, MTERFD1 and MTERFD3, as well as shRNA constructs targeted at each. We confirmed mitochondrial targeting and lack of sequence-specific DNA binding for both factors. Over-expression of epitope-tagged MTERFD1 or MTERFD3 resulted in modest mtDNA copy-number depletion and an accumulation of specific mtDNA replication intermediates indicating an impairment of the terminal steps of replication. These findings further implicate the mTERF family in restraining replication fork progression and support the idea that they facilitate the orderly passage of replication and transcription machineries, thus contributing to genome stability.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1573-4978
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1321-8
pubmed:dateRevised
2011-5-27
pubmed:meshHeading
pubmed:year
2011
pubmed:articleTitle
Overexpression of MTERFD1 or MTERFD3 impairs the completion of mitochondrial DNA replication.
pubmed:affiliation
Institute of Medical Technology and Centre for Laboratory Medicine, Tampere University Hospital, 33014, University of Tampere, Finland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't