Linked Life Data

12376559

Source:http://linkedlifedata.com/resource/pubmed/id/12376559

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
Pt 22
pubmed:dateCreated
2002-10-11
pubmed:abstractText
The mammalian Mat1 protein has been implicated in cell cycle regulation as part of the Cdk activating kinase (CAK), and in regulation of transcription as a subunit of transcription factor TFIIH. To address the role of Mat1 in vivo, we have used a Cre/loxP system to conditionally ablate Mat1 in adult mitotic and post-mitotic lineages. We found that the mitotic cells of the germ lineage died rapidly upon disruption of Mat1 indicating an absolute requirement of Mat1 in these cells. By contrast, post-mitotic myelinating Schwann cells were able to attain a mature myelinated phenotype in the absence of Mat1. Moreover, mutant animals did not show morphological or physiological signs of Schwann cell dysfunction into early adulthood. Beyond 3 months of age, however, myelinated Schwann cells in the sciatic nerves acquired a severe hypomyelinating morphology with alterations ranging from cells undergoing degeneration to completely denuded axons. This phenotype was coupled to extensive proliferation and remyelination that our evidence suggests was undertaken by the non-myelinated Schwann cell pool. These results indicate that Mat1 is not essential for the transcriptional program underlying the myelination of peripheral axons by Schwann cells and suggest that the function of Mat1 in RNA polymerase II-mediated transcription in these cells is regulatory rather than essential.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0021-9533
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
115
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4275-84
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12376559-Animals, pubmed-meshheading:12376559-Cell Division, pubmed-meshheading:12376559-Cell Lineage, pubmed-meshheading:12376559-Cyclin-Dependent Kinases, pubmed-meshheading:12376559-DNA-Binding Proteins, pubmed-meshheading:12376559-Early Growth Response Protein 2, pubmed-meshheading:12376559-Female, pubmed-meshheading:12376559-Gene Targeting, pubmed-meshheading:12376559-Genes, Regulator, pubmed-meshheading:12376559-Germ Cells, pubmed-meshheading:12376559-Male, pubmed-meshheading:12376559-Mice, pubmed-meshheading:12376559-Mice, Knockout, pubmed-meshheading:12376559-Microscopy, Electron, pubmed-meshheading:12376559-Myelin Sheath, pubmed-meshheading:12376559-Peripheral Nerves, pubmed-meshheading:12376559-Phenotype, pubmed-meshheading:12376559-Protein Subunits, pubmed-meshheading:12376559-RNA Polymerase II, pubmed-meshheading:12376559-Schwann Cells, pubmed-meshheading:12376559-Sciatic Nerve, pubmed-meshheading:12376559-Transcription Factor TFIIH, pubmed-meshheading:12376559-Transcription Factors, pubmed-meshheading:12376559-Transcription Factors, TFII, pubmed-meshheading:12376559-Wallerian Degeneration
pubmed:year
2002
pubmed:articleTitle
Conditional ablation of the Mat1 subunit of TFIIH in Schwann cells provides evidence that Mat1 is not required for general transcription.
pubmed:affiliation
Haartman Institute and Helsinki University Central Hospital, Biomedicum Helsinki, PO Box 63, Haartmaninkatu 8, 00014 University of Helsinki, Finland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't