Gene: Dmel\ttk
Ttk69, Tramtrack69, oversensitive, Ttk88, FTZ-F2
transcription factor - zinc finger - represses neural cell fate in the peripheral nervous system - a master repressor of enteroendocrine cell specification in intestinal stem cell lineages - regulates morphogenetic events during tracheal development
Please see the JBrowse view of Dmel\ttk for information on other features
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Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Gene model reviewed during 5.49
5.0, 4.2 (northern blot)
4.2 (longest cDNA)
813, 643 (aa); 88, 69 (kD predicted)
811, 641 (aa); 97 (kD observed); 88 (kD predicted)
641 (aa)
641 (aa); 69 (kD predicted)
ttk+P641 may repress expression of genes incompatible with the photoreceptor cell fate.
As absence of ttk+P811 correlates with supernumerary R7 photoreceptor cells, this protein may be required for suppression of genes which promote the R7 fate.
Although the ttk+P641 protein has a predicted molecular weight of 69kD, it runs at about 97 kD on a polyacrylamide-SDS gel. The zinc finger motifs, and the consensus DNA binding sites of the ttk+P881 and ttk+P641 proteins differ. The ttk+P641 protein binds sites in the eve promoter and autoregulatory element, while the ttk+P881 protein binds a region in the en promoter.
The ttk+P881 protein has a predicted molecular weight of 88 kD, although it runs about 50% slower than predicted on a polyacrylamide-SDS gel. The consensus DNA binding sites of the ttk+P881 and ttk+P641 proteins differ. The ttk+P641 protein binds sites in the eve promoter and autoregulatory element, while the ttk+P881 protein binds a region in the en promoter.
Can form homodimers (PubMed:12384587). Interacts with Trl in vivo via the BTB domain (PubMed:12384587). Interacts with phyl (PubMed:17962185). Interacts with Usp47 (PubMed:18160715).
Interacts with CoRest/CG33525, suggesting that it acts by recruiting a CoRest-containing corepressor complex. Interacts with phyl.
Polyubiquitinated by sina. Polyubiquitin linkage is mainly through 'Lys-48', but linkage through 'Lys-63' also occurs. Deubiquitination by Usp47 leads to its stabilization.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\ttk using the Feature Mapper tool.
Comment: maternally deposited
Comment: anlage in statu nascendi
Comment: specific to short isoform
Comment: 24 hr APF
Comment: reference states >=36 hr
Antibody specific to the smaller ttk isoform (referred to as Ttk69) detects expression in all epithelial cells, with the highest levels in enterocytes and the lowest levels in intestinal stem cells and enteroendocrine cells.
The 69 kD ttk protein isoform is expressed at low levels in follicle cells during stages S6-S9 of oogenesis, and at higher levels during stages S10A and S10B.
The 69 kD ttk protein is detected in the nucleus of all eight photoreceptor cells.
ttk protein expression is enriched in border follicle cells transiently at the beginning of migration. Border cell expression declines during migration. At stage 10, elevated expression becomes apparent in the centripetal cells as they initiate their inward migration. At late stages, high levels are detected in all oocyte-associated follicle cells.
69 kD ttk protein is expressed in embryonic glial cells later than repo protein. Highest expression of 69 kD ttk is observed when longitudinal glioblasts have migrated to their correct positions. 69 kD ttk is expressed in all mature glial cells of the embryonic central nervous system. 69 kD ttk is not detected in glioblasts undergoing DNA replication.
Both the 69 and 88 kD ttk protein isoforms are detected in pupal cone cells and pigment cells, but only the 69 kD isoform is detected in pupal photoreceptor cells.
GBrowse - Visual display of RNA-Seq signals
View Dmel\ttk in GBrowse 2
3-102
3-99.1
3-102.7
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 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.
polyclonal
Source for merge of: ttk CG1856
Source for merge of: ttk CG11558
DNA-protein interactions: genome-wide binding profile assayed for ttk protein in 0-12 hr embryos; see mE1_TFBS_ttk collection report.
dsRNA has been made from templates generated with primers directed against this gene. RNAi of ttk results in dorsal overextension of primary dendrites and a reduction in lateral branching. RNAi also causes alterations in the number of MD neurons, defects in dendrite morphogenesis and reproducible defects in da dendrite development.
ChEST reveals this is a target of Mef2.
ttk69 is required for dorsal appendage morphogenesis, but is not required fort cell fate determination.
Overexpression of ttk69 protein not only blocks neuronal photoreceptor differentiation but also promotes non-neural cone cell specification in early eye development.
The ttk isoform Ttk69, plays a positive and autonomous role in promoting and maintaining differentiation of photoreceptor neurons at the late stages of Drosophila eye development. ttk appears to have a dual function by serving negative and positive regulatory roles at different stages of photoreceptor development.
Identification: Enhancer trap expression pattern survey for loci expressed in the ring gland.
ttk is required for proper glial cell development in the CNS. Phenotypes of doubly mutant ttk and pnt embryos and ectopic expression of ttk and pnt indicates the existance of two independent genetic pathways regulating glial cell development, which in the lateral glia are both downstream of gcm. One, mediated via pnt, results in the activation of glia cell differentiation, whereas the other, mediated by ttk, results in the suppression of neuronal differentiation in these cells.
The role of ttk during sensory development is to impose the "non-neural" fate at each choice point during the lineage.
ttk has a role in the determination of different sensory organ precursor daughter cell fates. Loss of ttk function transforms support cells to neurons and overexpression results in the reverse transformation. Loss of ttk or numb function in sensory organ precursor daughter cells results in reciprocal cell fate transformation, epistatic studies suggest that ttk acts downstream of numb.
Removal of the POZ (poxvirus and zinc finger) domain increases DNA binding affinity of the chromosome.
Mutation in ttk affects the neuronal lineage, causes transformation of support cells into neurons.
ttk is required for PNS development in the embryo.
The highly complex pattern of ttk expression suggests specific functions for ttk late in development that are separate from the regulation of ftz. Ectopic ttk expression causes complete or near complete repression of ftz and significant repression of eve, odd, h and runt.
The structure of a two zinc finger DNA-binding domain from the ttk protein complexed with DNA is reported.
The structure of the DNA binding domain in complex with a specific binding site is determined.
ttk gene product is required for cell fate determination in the compound eye.
ttk has been cloned and sequenced. It is a zinc finger protein.
Gene encodes a zinc-finger protein binding to a number of sites involved in the transcriptional control of fushi-tarazu in the Antennapedia complex.
