Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
13
pubmed:dateCreated
2003-5-20
pubmed:abstractText
During the formation of the Drosophila heart, a combinatorial network that integrates signaling pathways and tissue-specific transcription factors specifies cardiac progenitors, which then undergo symmetric or asymmetric cell divisions to generate the final population of diversified cardiac cell types. Much has been learned concerning the combinatorial genetic network that initiates cardiogenesis, whereas little is known about how exactly these cardiac progenitors divide and generate the diverse population of cardiac cells. In this study, we examined the cell lineages and cell fate determination in the heart by using various cell cycle modifications. By arresting the cardiac progenitor cell divisions at different developing stages, we determined the exact cell lineages for most cardiac cell types. We found that once cardiac progenitors are specified, they can differentiate without further divisions. Interestingly, the progenitors of asymmetric cell lineages adopt a myocardial cell fate as opposed to a pericardial fate when they are unable to divide. These progenitors adopt a pericardial cell fate, however, when cell division is blocked in numb mutants or in embryos with constitutive Notch activity. These results suggest that a numb/Notch-dependent cell fate decision can take place even in undivided progenitors of asymmetric cell divisions. By contrast, in symmetric lineages, which give rise to a single type of myocardial-only or pericardial-only progeny, repression or constitutive activation of the Notch pathway has no apparent effect on progenitor or progeny fate. Thus, inhibition of Notch activity is crucial for specifying a myogenic cell fate only in asymmetric lineages. In addition, we provide evidence that whether or not Suppressor-of-Hairless can become a transcriptional activator is the key switch for the Numb/Notch activity in determining a myocardial versus pericardial cell fate.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/CycB protein, Drosophila, http://linkedlifedata.com/resource/pubmed/chemical/Cyclin A, http://linkedlifedata.com/resource/pubmed/chemical/Cyclin B, http://linkedlifedata.com/resource/pubmed/chemical/Drosophila Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Homeodomain Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Juvenile Hormones, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Notch, http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Fusion Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators, http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/eve protein, Drosophila, http://linkedlifedata.com/resource/pubmed/chemical/notch protein, Drosophila, http://linkedlifedata.com/resource/pubmed/chemical/numb protein, Drosophila, http://linkedlifedata.com/resource/pubmed/chemical/tin protein, Drosophila
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0950-1991
pubmed:author
pubmed:issnType
Print
pubmed:volume
130
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3039-51
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:12756185-Animals, pubmed-meshheading:12756185-Cell Cycle, pubmed-meshheading:12756185-Cell Division, pubmed-meshheading:12756185-Cell Lineage, pubmed-meshheading:12756185-Cyclin A, pubmed-meshheading:12756185-Cyclin B, pubmed-meshheading:12756185-Drosophila Proteins, pubmed-meshheading:12756185-Drosophila melanogaster, pubmed-meshheading:12756185-Enhancer Elements, Genetic, pubmed-meshheading:12756185-Heart, pubmed-meshheading:12756185-Homeodomain Proteins, pubmed-meshheading:12756185-Juvenile Hormones, pubmed-meshheading:12756185-Membrane Proteins, pubmed-meshheading:12756185-Mesoderm, pubmed-meshheading:12756185-Models, Biological, pubmed-meshheading:12756185-Morphogenesis, pubmed-meshheading:12756185-Myocardium, pubmed-meshheading:12756185-Receptors, Notch, pubmed-meshheading:12756185-Recombinant Fusion Proteins, pubmed-meshheading:12756185-Repressor Proteins, pubmed-meshheading:12756185-Signal Transduction, pubmed-meshheading:12756185-Stem Cells, pubmed-meshheading:12756185-Trans-Activators, pubmed-meshheading:12756185-Transcription Factors
pubmed:year
2003
pubmed:articleTitle
Myogenic cells fates are antagonized by Notch only in asymmetric lineages of the Drosophila heart, with or without cell division.
pubmed:affiliation
Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't