GAF, GAGA, GAGA factor, Nc70F, GAGA-factor
transcription factor - GAGA - Zinc finger - BTD domain - a chromatin modifying protein - cell division, dosage compensation and gametogenesis
Please see the JBrowse view of Dmel\Trl for information on other features
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Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.46
Gene model reviewed during 5.55
A non-AUG start codon may be used for translation of one or more transcripts of this gene; based on the presence of conserved protein signatures within the 5' UTR without an in-frame AUG (FBrf0243886).
120 (kD)
Interacts with Bin1, lolal, corto, ttk and ph-p (PubMed:11256608, PubMed:12384587, PubMed:12834867, PubMed:12771214). Interacts with FACT subunits Ssrp and dre4/SPT16 (PubMed:12815073). Interacts with E(bx) (PubMed:11583616). Upon ecdysone stimulation, interacts with Nup98 (PubMed:28366641).
The N-terminus is blocked.
The N-terminal BTB domain mediates protein oligomerization. The C-terminal glutamine-rich region is required for transcriptional activation activity.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Trl using the Feature Mapper tool.
Comment: maternally deposited
Comment: reported as muscle system primordium
Comment: reported as muscle system primordium
Trl protein is localized to the nuclei of all cell types in the pupal retina
GBrowse - Visual display of RNA-Seq signals
View Dmel\Trl in GBrowse 2
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 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: Trl CG9343
Source for merge of: Trl anon- EST:fe2E12
Source for merge of: Trl Nc70F
This gene was originally designated as 'trithorax-like' ('Trl') residing in the left arm of the third chromosome, based on the observation that some mutant alleles could cause homeotic transformations like mutations in trx (FBrf0076985). However, this assignment is not supported by subsequent reports (FBrf0107412, FBrf0155709). Indeed, the homeotic effect is lost when the right arm of the third chromosome of the original alleles is replaced by a genetically marked WT chromosome (unpublished data). To avoid potential confusion, we refer to the gene as 'GAGA factor' ('Gaf').
Annotation CG33260 has been re-extended to its original form (corresponding to the annotation originally named CG13470) in release 5.1 of the genome annotation. The 3' end of release 5.1 annotation CG33260 (including some of the CDS) overlaps the 5' UTR of the neighbouring release 5.1 Trl annotation which is on the same strand.
Source for merge of Trl Nc70F was sequence comparison ( date:000202 ).
DNA-protein interactions: genome-wide binding profile assayed for Trl protein in 0-12 hr embryos; see mE1_TFBS_Trl collection report.
DNA-protein interactions: genome-wide binding profile assayed for Trl protein in Kc167 cells; see Chromatin_types_NKI collection report. Individual protein-binding experiments listed under "Samples" at GEO_GSE22069 (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE22069).
DNA-protein interactions: genome-wide binding profile assayed for Trl protein in 0-12 hr embryos. Individual protein-binding experiments listed under "Samples" at GEO: 16245 (http://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE16245).
RNAi generated by PCR using primers directed to this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R+ cells.
RNAi screen using dsRNA made from templates generated with primers directed against this gene causes a cell growth and viability phenotype when assayed in Kc167 and S2R+ cells.
Trl is required for dosage compensation in males.
Genetic interaction data suggest that Trl may have a role in control of homeotic gene activity.
Trl protein forms oligomers both in vitro and in vivo. The formation of these oligomers, which exist in solution in the absence of DNA binding, requires the N-terminal POZ domain.
Two major primary isoforms of Trl are identified, GAGA-519 and GAGA-581. The isoforms share an N-terminal protein-protein interaction domain and a DNA binding domain, but differ in their C-termini. Both isoforms exhibit a full spectrum of biological activities.
The Trl gene product is required for a variety of developmental loci that contain GAGA binding sites in their upstream regulatory regions. The effects of mutation in Trl are consistent with a role in chromatin remodeling. Other defects suggest an additional, more global role in chromosome structure and function, related to the association of the GAGA protein with heterochromatic satellite sequences observed throughout the cell cycle.
The single zinc finger domain from the Trl protein, along with a stretch of amino acids at the N terminus of the finger, is sufficient for specific DNA binding.
UV cross linking technique has been used to study the in vivo distribution of Trl protein on Hsp70 and Hsp26. Prior to heat shock Trl protein is associated with the promoter regions of the uninduced Hsp70 and Hsp26 genes. Upon heat shock induction Trl protein is recruited to their transcription units with its distribution coincident with that of RNA polymerase II.
Nucleosome remodelling factor is composed of at least four polypeptides that act in concert with the Trl transcription factor at the Hsp70 promoter.
Removal of the POZ (poxvirus and zinc finger) domain increases DNA binding affinity of the chromosome.
Trl encodes the GAGA factor which is involved in the formation of an accessible chromatin structure at promoter sequences.
Trl is associated with regions of heterochromatin throughout the cell cycle, probably via a direct interaction with a GA/CT rich subset of the highly repetitive DNA sequences found in heterochromatin. Trl can also associate with specific DNA sequences even when the DNA is highly compacted in the mitotic chromosomes.
Introduction of Trl protein during or after nucleosome assembly in vitro results in disruption of nucleosome structure at the Hsp70Aa promoter. Hsp70Aa promoter deletion analysis reveals that disruption of a preassembled nucleosome requires three or four GA/CT elements, nucleosome displacement requires at least two GA/CT elements.
Trl promotes chromatin rearrangement at heat shock loci.
The Trl gene product is a multipurpose transcriptional activator which binds to (GA/CT)n sites in a host of promoters.
