The Little Elongation Complex Regulates Small Nuclear RNA Transcription

Eleven-nineteen lysine-rich leukemia (ELL) participates in the super elongation complex (SEC) with the RNA polymerase II (Pol II) CTD kinase P-TEFb. SEC is a key regulator in the expression of HOX genes in mixed lineage leukemia (MLL)-based hematological malignancies, in the control of induced gene...

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Veröffentlicht in:Molecular cell 2011-12, Vol.44 (6), p.954-965
Hauptverfasser: Smith, Edwin R., Lin, Chengqi, Garrett, Alexander S., Thornton, Janet, Mohaghegh, Nima, Hu, Deqing, Jackson, Jessica, Saraf, Anita, Swanson, Selene K., Seidel, Christopher, Florens, Laurence, Washburn, Michael P., Eissenberg, Joel C., Shilatifard, Ali
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Sprache:eng
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Zusammenfassung:Eleven-nineteen lysine-rich leukemia (ELL) participates in the super elongation complex (SEC) with the RNA polymerase II (Pol II) CTD kinase P-TEFb. SEC is a key regulator in the expression of HOX genes in mixed lineage leukemia (MLL)-based hematological malignancies, in the control of induced gene expression early in development, and in immediate early gene transcription. Here, we identify an SEC-like complex in Drosophila, as well as a distinct ELL-containing complex that lacks P-TEFb and other components of SEC named the “little elongation complex” (LEC). LEC subunits are highly enriched at RNA Pol II-transcribed small nuclear RNA (snRNA) genes, and the loss of LEC results in decreased snRNA expression in both flies and mammals. The specialization of the SEC and LEC complexes for mRNA and snRNA-containing genes, respectively, suggests the presence of specific classes of elongation factors for each class of genes transcribed by RNA polymerase II. ► ELL's conserved C-terminal domain interacts with ICE1 and ICE2 ► ELL and ICE1 and ICE2 form a complex, named LEC, distinct from the P-TEFb-containing SEC ► In both Drosophila and mammalian cells, LEC, but not SEC, is enriched at snRNA genes ► LEC is required for Pol II-mediated snRNA transcription in flies and mammals
ISSN:1097-2765
1097-4164
DOI:10.1016/j.molcel.2011.12.008