Linked Life Data

7649393

Source:http://linkedlifedata.com/resource/pubmed/id/7649393

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1995-9-25
pubmed:abstractText
Asymmetric cell divisions in which a precursor cell distributes fate potential unequally between the two daughter cells represent one of the major mechanisms for fate specification during development. Such mechanisms suggest at least two distinct cellular activities: factors that act to establish asymmetry in the precursor cell and factors that are distributed or activated unequally and function to make the daughter cells different from each other. In Caenorhabditis elegans, cytokinesis of the first division of the male-specific postembryonic blast cell B is unequal, and the two daughters adopt different fates. Others have observed that the genes lin-17 and lin-44 are required, respectively, to establish and to orient this asymmetric division. Mutations in lin-17 and lin-44 coordinately disrupt cytokinesis and fate specification. We describe the function of the gene vab-3 in the B cell lineage. Mutations in vab-3 disrupt the fate of the anterior daughter of B, B.a. However, unlike lin-17 and lin-44, mutations in vab-3 can disrupt fate without the corresponding disruption of unequal cytokinesis. Analysis of lin-17;vab-3 double mutants suggests that vab-3 acts after lin-17 for B.a. fate specification. Double mutant analysis has also identified additional functions of lin-17 in the B lineage subsequent to this first division.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0012-1606
pubmed:author
pubmed:issnType
Print
pubmed:volume
170
pubmed:geneSymbol
vab-3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
679-89
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
Mutations in the Caenorhabditis elegans gene vab-3 reveal distinct roles in fate specification and unequal cytokinesis in an asymmetric cell division.
pubmed:affiliation
Howard Hughes Medical Institute, Division of Biology, California Institute of Technology, Pasadena 91125, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't