P-TEFb, Positive transcription elongation factor b
Gene model reviewed during 5.51
There is only one protein coding transcript and one polypeptide associated with this gene
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Cdk9 using the Feature Mapper tool.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Cdk9 in GBrowse 2
Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.
For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.
Source for identity of: Cdk9 CG5179
Identified as a potential component of the hh signalling pathway in a genome-wide RNAi screen. dsRNA made from templates generated with primers directed affects the extent of expression of a hh signaling reporter construct in Clone 8 cells.
When dsRNA constructs are made and transiently transfected into S2 cells in RNAi experiments, an increase in the proportion of G1 phase cells and a decrease in the mitotic index are seen.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
RNAi screen using dsRNA made from templates generated with primers directed against this gene causes a phenotype when assayed in Kc167 and S2R+ cells: cells become round and detached, cell morphology is aberrant and there is an increased frequency of microtubule-based mitotic spindles, indicative of a failure in mitosis.
Area matching Drosophila Positive transcription elongation factor b, Acc. No. AF027300. Probable intron.
Cdk9 is cloned and identified as the counterpart of two human protein kinases. Purified P-TEFb can functionally replace the transcriptional activity removed from HeLa extract with human PITALRE antibodies.
Removal of the carboxy terminal domain (CTD) of the large subunit of RNA polymerase II (RpII215) abolished productive elongation. P-TEFb can phosphorylate the CTD. Both function and kinase activity of P-TEFb can be blocked by application of drugs. TfIIH cannot substitute for P-TEFb. Phosphorylation of the CTD by P-TEFb controls the transition from abortive into productive elongation mode.
P-TEFb stimulates the level of runoff transcripts in vitro.