Linked Life Data

8404530

Source:http://linkedlifedata.com/resource/pubmed/id/8404530

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1993-11-16
pubmed:abstractText
An interaction between the two principal populations of mesodermal cells in the sea urchin embryo, primary and secondary mesenchyme cells (PMCs and SMCs, respectively), regulates SMC fates and the process of skeletogenesis. In the undisturbed embryo, skeletal elements are produced exclusively by PMCs. Certain SMCs also have the ability to express a skeletogenic phenotype; however, signals transmitted by the PMCs direct these cells into alternative developmental pathways. In this study, a combination of fluorescent cell-labeling methods, embryo microsurgery and cell-specific molecular markers have been used to study the lineage, numbers, normal fate(s) and developmental potential of the skeletogenic SMCs. Previous fate-mapping studies have shown that SMCs are derived from the veg2 layer of blastomeres of the 64-cell-stage embryo and from the small micromeres. By specifically labeling the small micromeres with 5-bromodeoxyuridine, we demonstrate that descendants of these cells do not participate in skeletogenesis in PMC-depleted larvae, even though they are the closest lineal relatives of PMCs. Skeletogenic SMCs are therefore derived exclusively from the veg2 blastomeres. Because the SMCs are a heterogeneous population of cells, we have sought to gain information concerning the normal fate(s) of skeletogenic SMCs by determining whether specific cell types are reduced or absent in PMC(-) larvae. Of the four known SMC derivatives: pigment cells, blastocoelar (basal) cells, muscle cells and coelomic pouch cells, only pigment cells show a major reduction (> 50%) in number following SMC skeletogenesis. We therefore propose that the PMC-derived signal regulates a developmental switch, directing SMCs to adopt a pigment cell phenotype instead of a default (skeletogenic) fate. Ablation of SMCs at the late gastrula stage does not result in the recruitment of any additional skeletogenic cells, demonstrating that, by this stage, the number of SMCs with skeletogenic potential is restricted to 60-70 cells. Previous studies showed that during their switch to a skeletogenic fate, SMCs alter their migratory behavior and cell surface properties. In this study, we demonstrate that during conversion, SMCs become insensitive to the PMC-derived signal, while at the same time they acquire PMC-specific signaling properties.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0950-1991
pubmed:author
pubmed:issnType
Print
pubmed:volume
117
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1275-85
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1993
pubmed:articleTitle
Mesodermal cell interactions in the sea urchin embryo: properties of skeletogenic secondary mesenchyme cells.
pubmed:affiliation
Department of Biological Sciences and Center for Light Microscope Imaging and Biotechnology, Carnegie Mellon University, Pittsburgh, PA 15213.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.