| pubmed-article:18200011 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18200011 | lifeskim:mentions | umls-concept:C0231044 | lld:lifeskim |
| pubmed-article:18200011 | lifeskim:mentions | umls-concept:C0008546 | lld:lifeskim |
| pubmed-article:18200011 | lifeskim:mentions | umls-concept:C0663446 | lld:lifeskim |
| pubmed-article:18200011 | lifeskim:mentions | umls-concept:C0271510 | lld:lifeskim |
| pubmed-article:18200011 | lifeskim:mentions | umls-concept:C2352048 | lld:lifeskim |
| pubmed-article:18200011 | pubmed:issue | 7179 | lld:pubmed |
| pubmed-article:18200011 | pubmed:dateCreated | 2008-2-7 | lld:pubmed |
| pubmed-article:18200011 | pubmed:abstractText | Germ cells are the only cells that transmit genetic information to the next generation, and they therefore must be prevented from differentiating inappropriately into somatic cells. A common mechanism by which germline progenitors are protected from differentiation-inducing signals is a transient and global repression of RNA polymerase II (RNAPII)-dependent transcription. In both Drosophila and Caenorhabditis elegans embryos, the repression of messenger RNA transcription during germ cell specification correlates with an absence of phosphorylation of Ser 2 residues in the carboxy-terminal domain of RNAPII (hereafter called CTD), a critical modification for transcriptional elongation. Here we show that, in Drosophila embryos, a small protein encoded by polar granule component (pgc) is essential for repressing CTD Ser 2 phosphorylation in newly formed pole cells, the germline progenitors. Ectopic Pgc expression in somatic cells is sufficient to repress CTD Ser 2 phosphorylation. Furthermore, Pgc interacts, physically and genetically, with positive transcription elongation factor b (P-TEFb), the CTD Ser 2 kinase complex, and prevents its recruitment to transcription sites. These results indicate that Pgc is a cell-type-specific P-TEFb inhibitor that has a fundamental role in Drosophila germ cell specification. In C. elegans embryos, PIE-1 protein segregates to germline blastomeres, and is thought to repress mRNA transcription through interaction with P-TEFb. Thus, inhibition of P-TEFb is probably a common mechanism during germ cell specification in the disparate organisms C. elegans and Drosophila. | lld:pubmed |
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| pubmed-article:18200011 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:18200011 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18200011 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18200011 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:18200011 | pubmed:issn | 1476-4687 | lld:pubmed |
| pubmed-article:18200011 | pubmed:author | pubmed-author:NakamuraAkira... | lld:pubmed |
| pubmed-article:18200011 | pubmed:author | pubmed-author:LaskoPaulP | lld:pubmed |
| pubmed-article:18200011 | pubmed:author | pubmed-author:TanigawaAkieA | lld:pubmed |
| pubmed-article:18200011 | pubmed:author | pubmed-author:Hanyu-Nakamur... | lld:pubmed |
| pubmed-article:18200011 | pubmed:author | pubmed-author:Sonobe-Nojima... | lld:pubmed |
| pubmed-article:18200011 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18200011 | pubmed:day | 7 | lld:pubmed |
| pubmed-article:18200011 | pubmed:volume | 451 | lld:pubmed |
| pubmed-article:18200011 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18200011 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18200011 | pubmed:pagination | 730-3 | lld:pubmed |
| pubmed-article:18200011 | pubmed:dateRevised | 2011-5-4 | lld:pubmed |
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| pubmed-article:18200011 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:18200011 | pubmed:articleTitle | Drosophila Pgc protein inhibits P-TEFb recruitment to chromatin in primordial germ cells. | lld:pubmed |
| pubmed-article:18200011 | pubmed:affiliation | Laboratory for Germline Development, RIKEN Center for Developmental Biology, Kobe, Hyogo 650-0047, Japan. | lld:pubmed |
| pubmed-article:18200011 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:18200011 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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