RNA polymerase II, RpII140, DmRP140, wimp, PolII
Please see the JBrowse view of Dmel\Polr2B for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
AlphaFold produces a per-residue confidence score (pLDDT) between 0 and 100. Some regions with low pLDDT may be unstructured in isolation.
Gene model reviewed during 5.54
Component of the RNA polymerase II (Pol II) complex consisting of 12 subunits.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Polr2B using the Feature Mapper tool.
The testis specificity index was calculated from modENCODE tissue expression data by Vedelek et al., 2018 to indicate the degree of testis enrichment compared to other tissues. Scores range from -2.52 (underrepresented) to 5.2 (very high testis bias).
Comment: maternally deposited
JBrowse - Visual display of RNA-Seq signals
View Dmel\Polr2B in JBrowse3-54
3-52.7
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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 JBrowse 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.
polyclonal
DNA-protein interactions: genome-wide binding profile (ChIP-chip) assayed for PolII holoenzyme in adult heads; see GEO_GSE32613 (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE32613).
Suppressor mutations isolated on the basis of restoring viability to RpII215 and RpII140 mutants identify discrete domains in either subunit. The suppressor domain is required for viability and functioning of RNA polymerase II. The mutations recovered are not random and might provide insights into possible mechanisms for mutagenesis in eukaryotes.
Used in a phylogenetic analysis, the tree in inferred by parsimony method from RpoB sequences, or homologous, multiple alignment.
Deletion analysis of the RpII140 protein shows that a region in the N-terminal part of the protein (amino acids 357-504) shows strong DNA binding, and the C-terminal part of the protein (amino acids 860-1160) shows some weak DNA binding.
Upstream of RpII140 is a gene, 140up, which is transcribed in the opposite direction. Both genes are characterised by multiple transcription start sites. Gel retardation assays with in vitro transcribed and translated Tbp reveals two regions in the RpII140 promoter region that bind Tbp. Transient transfection assays with Tbp and Ecol\CAT driven by the RpII140 promoter result in 2-3 fold increase in Ecol\CAT activity, promoter deletion analysis identifies three regions important for transcription.
The technique of paramagnetic particle-mediated selection of terminated run-on transcripts was used to examine RNA polymerase II pausing and 5' cap formation at high resolution on the heat shock genes Hsp70A, Hsp70B, Hsp26 and Hsp27. Results demonstrate that polymerases pause over a narrow region of each heat shock gene, not at a defined point. 5' capping occurs over a region coincidental with that of pausing.
Protein complexes of RNA polymerase II localise to major developmental puffs and heat shock puffs.
Three RpII140 alleles cause a dominant enhancement of the Ubx effect: transformation of the capitellum to wing. The alleles do not enhance the Ubx effect of RpII15 alleles.
RpII140 has been cloned and sequenced.
The structural gene for the 140kD subunit of RNA polymerase II (RNA nucleotidyl transferase). The gene is highly conserved judging from shared sequence homology with the yeast 150kD subunit gene.
Source for merge of: RpII140 Rpb2
Mutants selected by Mortin, (1990) as extragenic suppressors of RpII215K1.
Source for identity of: Polr2B RpII140
Named 'Polr2B' after the human ortholog.
