Linked Life Data

19368799

Source:http://linkedlifedata.com/resource/pubmed/id/19368799

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5-6
pubmed:dateCreated
2009-5-11
pubmed:abstractText
Dividing stem cells can give rise to two types of daughter cells; self-renewing cells that have virtually the same properties as the parent cell, and differentiating cells that will eventually form part of a tissue. The Caenorhabditis elegans germ line serves as a model to study how the balance between these two types of daughter cells is maintained. A mutation in teg-4 causes over-proliferation of the stem cells, thereby disrupting the balance between proliferation and differentiation. We have cloned teg-4 and found it to encode a protein homologous to the highly conserved splicing factor subunit 3 of SF3b. Our allele of teg-4 partially reduces TEG-4 function. In an effort to determine how teg-4 functions in controlling stem cell proliferation, we have performed genetic epistasis analysis with known factors controlling stem cell proliferation. We found that teg-4 is synthetic tumorous with genes in both major redundant genetic pathways that function downstream of GLP-1/Notch signaling to control the balance between proliferation and differentiation. Therefore, teg-4 is unlikely to function specifically in either of these two genetic pathways. Further, the synthetic tumorous phenotype seen with one of the genes from these pathways is epistatic to glp-1, indicating that teg-4 functions downstream of glp-1, likely as a positive regulator of meiotic entry. We propose that a reduction in teg-4 activity reduces the splicing efficiency of targets involved in controlling the balance between proliferation and differentiation. This results in a shift in the balance towards proliferation, eventually forming a germline tumor.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1872-6356
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
126
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
417-29
pubmed:meshHeading
pubmed-meshheading:19368799-Alleles, pubmed-meshheading:19368799-Amino Acid Sequence, pubmed-meshheading:19368799-Animals, pubmed-meshheading:19368799-Caenorhabditis elegans, pubmed-meshheading:19368799-Caenorhabditis elegans Proteins, pubmed-meshheading:19368799-Cell Differentiation, pubmed-meshheading:19368799-Cell Proliferation, pubmed-meshheading:19368799-Embryo, Nonmammalian, pubmed-meshheading:19368799-Epistasis, Genetic, pubmed-meshheading:19368799-Germ Cells, pubmed-meshheading:19368799-Larva, pubmed-meshheading:19368799-Membrane Glycoproteins, pubmed-meshheading:19368799-Molecular Sequence Data, pubmed-meshheading:19368799-Mutation, pubmed-meshheading:19368799-Phenotype, pubmed-meshheading:19368799-Protein Subunits, pubmed-meshheading:19368799-RNA Precursors, pubmed-meshheading:19368799-RNA-Binding Proteins, pubmed-meshheading:19368799-Receptors, Notch, pubmed-meshheading:19368799-Sequence Homology, Amino Acid, pubmed-meshheading:19368799-Signal Transduction, pubmed-meshheading:19368799-Temperature
pubmed:articleTitle
A mutation in teg-4, which encodes a protein homologous to the SAP130 pre-mRNA splicing factor, disrupts the balance between proliferation and differentiation in the C. elegans germ line.
pubmed:affiliation
Department of Biological Sciences, University of Calgary, Alberta, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural