TFIID is a DNA-binding protein
complex required for RNA polymerase II-mediated transcription of many, if not all, protein-encoding genes in
eukaryotic cells. The largest subunit of the human transcription factor TFIID, TAFII250, contains serine/threonine kinase domains that
can autophosphorylate and transphosphorylate the large subunit of the basal factor TFIIF.
NCBI Summary:
Initiation of transcription by RNA polymerase II requires the activities of more than 70 polypeptides. The protein that coordinates these activities is the basal transcription factor TFIID, which binds to the core promoter to position the polymerase properly, serves as the scaffold for assembly of the remainder of the transcription complex, and acts as a channel for regulatory signals. TFIID is composed of the TATA-binding protein (TBP) and a group of evolutionarily conserved proteins known as TBP-associated factors or TAFs. TAFs may participate in basal transcription, serve as coactivators, function in promoter recognition or modify general transcription factors (GTFs) to facilitate complex assembly and transcription initiation. This gene encodes the largest subunit of TFIID. This subunit binds to core promoter sequences encompassing the transcription start site. It also binds to activators and other transcriptional regulators, and these interactions affect the rate of transcription initiation. This subunit contains two independent protein kinase domains at the N and C-terminals, but also possesses acetyltransferase activity and can act as a ubiquitin-activating/conjugating enzyme. Two transcripts encoding different isoforms have been identified for this gene.
General function
DNA binding, Transcription factor
Comment
Cellular localization
Nuclear
Comment
Freiman et al. (2001) reported that the tissue-selective TAFII105 subunit of TFIID is essential for proper development and function of the
mouse ovary. They also demonstrated the expression of TAFII 250 subunit expression in the ovary. Female mice lacking TAFII105 are viable but infertile because of a defect in folliculogenesis correlating with
restricted expression of TAFII105 in the granulosa cells of the ovarian follicle. Gene expression profiling has uncovered a
defective inhibin-activin signaling pathway in TAFII105-deficient ovaries. These studies suggest that TAFII105 mediates
the transcription of a subset of genes required for proper folliculogenesis in the ovary and establishes TAFII105 as a cell
type-specific component of the mammalian transcriptional machinery.