Reference Report

Reference
Citation	Hanyu-Nakamura, K., Sonobe-Nojima, H., Tanigawa, A., Lasko, P., Nakamura, A. (2008). Drosophila Pgc protein inhibits P-TEFb recruitment to chromatin in primordial germ cells. Nature 451(7179): 730--733. (Export to RIS)
FlyBase ID	FBrf0202665
Publication Type	Research paper
PubMed ID	18200011
PubMed Abstract	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.
DOI	10.1038/nature06498
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Secondary IDs	FBrf0204342
Language of Publication	English
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Publication Type	Journal
Abbreviation	Nature
Title	Nature
Publication Year	1869-
ISBN/ISSN	0028-0836
Data from Reference
Aberrations (2)
	Df(2R)pgc^Δ1 Df(2R)X58-7
Alleles (13)
	Cdk9^{nos.3'UTR.Scer\UAS.P\T} CycT^{nos.3'UTR.Scer\UAS.P\T} Gp150^+t17.5 pgc^{bcd.3'UTR.Scer\UAS.P\T} pgc^{fs.Scer\UAS.P\T} pgc^{gcl.3'UTR.Scer\UAS.P\T} pgc^{nos.3'UTR.Scer\UAS.P\T} pgc^{Scer\UAS.cHNa} pgc^{Scer\UAS.P\T.cHNa} pgc^T:Zzzz\FLAG Scer\GAL4^{nos.UTR.T:Hsim\VP16} Scer\GAL4^Sgs3.PD w^+mC
Constructs (13)
	P{GAL4::VP16-nos.UTR} P{Gp150^+t17.5} P{pgc^T:Zzzz\FLAG} P{PZ} P{Sgs3-GAL4.PD} P{UASp-Cdk9.nos-3'UTR} P{UASp-CycT.nos-3'UTR} P{UASp-pgc.bcd-3'UTR} P{UASp-pgc.fs} P{UASp-pgc.gcl-3'UTR} P{UASp-pgc.HN} P{UASp-pgc.nos-3'UTR} P{UAST-pgc.HN}
Genes (30)
	Cdk7 Cdk9 CycT Dana\pgc Dere\pgc Dgri\pgc Dmoj\pgc Dper\pgc Dpse\pgc Dsec\pgc Dsim\pgc Dvir\pgc Dwil\pgc Dyak\pgc eve ftz Gp150 Hsp27 Hsp70Aa Hsp70Ab Hsp70Ba Hsp70Bb Hsp70Bbb Hsp70Bc pgc RpII215 Scer\GAL4 T3dh T:Zzzz\FLAG w
Insertions (1)
	P{PZ}rF139
Natural transposons (1)
	P-element