| pubmed-article:17567664 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17567664 | lifeskim:mentions | umls-concept:C0105770 | lld:lifeskim |
| pubmed-article:17567664 | lifeskim:mentions | umls-concept:C0013936 | lld:lifeskim |
| pubmed-article:17567664 | lifeskim:mentions | umls-concept:C0013126 | lld:lifeskim |
| pubmed-article:17567664 | lifeskim:mentions | umls-concept:C1160042 | lld:lifeskim |
| pubmed-article:17567664 | lifeskim:mentions | umls-concept:C0162610 | lld:lifeskim |
| pubmed-article:17567664 | lifeskim:mentions | umls-concept:C1706942 | lld:lifeskim |
| pubmed-article:17567664 | lifeskim:mentions | umls-concept:C0332514 | lld:lifeskim |
| pubmed-article:17567664 | lifeskim:mentions | umls-concept:C1882911 | lld:lifeskim |
| pubmed-article:17567664 | pubmed:issue | 14 | lld:pubmed |
| pubmed-article:17567664 | pubmed:dateCreated | 2007-6-26 | lld:pubmed |
| pubmed-article:17567664 | pubmed:abstractText | C. elegans embryos exhibit an invariant lineage comprised primarily of a stepwise binary diversification of anterior-posterior (A-P) blastomere identities. This binary cell fate specification requires input from both the Wnt and MAP kinase signaling pathways. The nuclear level of the TCF protein POP-1 is lowered in all posterior cells. We show here that the beta-catenin SYS-1 also exhibits reiterated asymmetry throughout multiple A-P divisions and that this asymmetry is reciprocal to that of POP-1. Furthermore, we show that SYS-1 functions as a coactivator for POP-1, and that the SYS-1-to-POP-1 ratio appears critical for both the anterior and posterior cell fates. A high ratio drives posterior cell fates, whereas a low ratio drives anterior cell fates. We show that the SYS-1 and POP-1 asymmetries are regulated independently, each by a subset of genes in the Wnt/MAP kinase pathways. We propose that two genetic pathways, one increasing SYS-1 and the other decreasing POP-1 levels, robustly elevate the SYS-1-to-POP-1 ratio in the posterior cell, thereby driving A-P differential cell fates. | lld:pubmed |
| pubmed-article:17567664 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17567664 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17567664 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17567664 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17567664 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:17567664 | pubmed:issn | 0950-1991 | lld:pubmed |
| pubmed-article:17567664 | pubmed:author | pubmed-author:LinRueylingR | lld:pubmed |
| pubmed-article:17567664 | pubmed:author | pubmed-author:RobertsonScot... | lld:pubmed |
| pubmed-article:17567664 | pubmed:author | pubmed-author:ShettyPremnat... | lld:pubmed |
| pubmed-article:17567664 | pubmed:author | pubmed-author:HuangShuyiS | lld:pubmed |
| pubmed-article:17567664 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17567664 | pubmed:volume | 134 | lld:pubmed |
| pubmed-article:17567664 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17567664 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17567664 | pubmed:pagination | 2685-95 | lld:pubmed |
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| pubmed-article:17567664 | pubmed:meshHeading | pubmed-meshheading:17567664... | lld:pubmed |
| pubmed-article:17567664 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17567664 | pubmed:articleTitle | Binary cell fate specification during C. elegans embryogenesis driven by reiterated reciprocal asymmetry of TCF POP-1 and its coactivator beta-catenin SYS-1. | lld:pubmed |
| pubmed-article:17567664 | pubmed:affiliation | Department of Molecular Biology, University of Texas Southwestern Medical Center, 6000 Harry Hines Boulevard, Dallas, TX 75390, USA. | lld:pubmed |
| pubmed-article:17567664 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17567664 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17567664 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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