| pubmed-article:15380620 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15380620 | lifeskim:mentions | umls-concept:C0870134 | lld:lifeskim |
| pubmed-article:15380620 | lifeskim:mentions | umls-concept:C0027882 | lld:lifeskim |
| pubmed-article:15380620 | lifeskim:mentions | umls-concept:C0521329 | lld:lifeskim |
| pubmed-article:15380620 | lifeskim:mentions | umls-concept:C1442161 | lld:lifeskim |
| pubmed-article:15380620 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:15380620 | lifeskim:mentions | umls-concept:C0205164 | lld:lifeskim |
| pubmed-article:15380620 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
| pubmed-article:15380620 | lifeskim:mentions | umls-concept:C1881379 | lld:lifeskim |
| pubmed-article:15380620 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:15380620 | pubmed:dateCreated | 2004-9-21 | lld:pubmed |
| pubmed-article:15380620 | pubmed:abstractText | Vertebrate embryos are able to reconstitute the body plan when early blastomeres are deleted, but it is not known whether this is accomplished by cells local to the lesion or by a readjustment of the entire pattern of the embryo. We distinguished between these two possibilities by studying which embryonic cells change primary spinal neuronal fates after deletion of a major spinal cord progenitor. After ablation of the V1.2 blastomere of the 16-cell Xenopus embryo, the spinal cord contained normal numbers of Rohon-Beard neurons and primary motoneurons, indicating that the remaining blastomeres numerically reconstituted these populations. Using lineage-tracing techniques we revealed a global response: 10 out of the 15 remaining blastomeres significantly changed the number of one or both neuronal types they produced. This widespread response indicates that position in the early embryo plays an important role in regulating the production of primary spinal neurons. However, not all cells are influenced solely by position; a vegetal cell transplanted into the position of the deleted V1.2 did not take on the neuronal fate of its new position. Thus, restitution of pattern relies on a combination of positional cues and intrinsic fate restrictions. | lld:pubmed |
| pubmed-article:15380620 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15380620 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15380620 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15380620 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15380620 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15380620 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15380620 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:15380620 | pubmed:issn | 0248-4900 | lld:pubmed |
| pubmed-article:15380620 | pubmed:author | pubmed-author:MoodySally... | lld:pubmed |
| pubmed-article:15380620 | pubmed:author | pubmed-author:GallagherBett... | lld:pubmed |
| pubmed-article:15380620 | pubmed:copyrightInfo | Copyright 2004 Elsevier SAS | lld:pubmed |
| pubmed-article:15380620 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15380620 | pubmed:volume | 96 | lld:pubmed |
| pubmed-article:15380620 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15380620 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15380620 | pubmed:pagination | 539-44 | lld:pubmed |
| pubmed-article:15380620 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:15380620 | pubmed:meshHeading | pubmed-meshheading:15380620... | lld:pubmed |
| pubmed-article:15380620 | pubmed:meshHeading | pubmed-meshheading:15380620... | lld:pubmed |
| pubmed-article:15380620 | pubmed:meshHeading | pubmed-meshheading:15380620... | lld:pubmed |
| pubmed-article:15380620 | pubmed:meshHeading | pubmed-meshheading:15380620... | lld:pubmed |
| pubmed-article:15380620 | pubmed:meshHeading | pubmed-meshheading:15380620... | lld:pubmed |
| pubmed-article:15380620 | pubmed:meshHeading | pubmed-meshheading:15380620... | lld:pubmed |
| pubmed-article:15380620 | pubmed:meshHeading | pubmed-meshheading:15380620... | lld:pubmed |
| pubmed-article:15380620 | pubmed:meshHeading | pubmed-meshheading:15380620... | lld:pubmed |
| pubmed-article:15380620 | pubmed:meshHeading | pubmed-meshheading:15380620... | lld:pubmed |
| pubmed-article:15380620 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15380620 | pubmed:articleTitle | Regulation of primary spinal neuron lineages after deletion of a major progenitor. | lld:pubmed |
| pubmed-article:15380620 | pubmed:affiliation | University of Virginia, Department of Molecular Physiology and Biological Physics, Charlottesville, VA, USA. | lld:pubmed |
| pubmed-article:15380620 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15380620 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:15380620 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
