yan, pokkuri, pok, DROYANETSB, aop/yan
ets domain transcription factor - target of Ras pathway that serves to inhibit neural and other types of differentiation - crucial to the development of the nervous system, heart, trachea and eye
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Gene model reviewed during 5.44
Gene model reviewed during 5.47
Phosphorylated in response to MAPK signaling. May be phosphorylated by rl.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\aop using the Feature Mapper tool.
aop expression is observed in the Bolwig organ primordium from embryonic stage 10/11 to stage 12/13 and is gone by stage 15.
aop protein is not detected in embryos until the germ band is fully extended. At stage 10, it is expressed in most regions of the epidermis. During germ band retraction, expression is gradually restricted. By stage 13, there are only 40-50 aop-positive cells that appear to correspond to most of the cells of the tracheal system. In third instar larvae, expression is observed in the eye disc but not in other discs. aop is expressed in most nuclei near the morphogenetic furrow, throughout the depth of the epithelium. Posterior to the furrow, only uncommitted cells express aop. As cells begin to differentiate, their nuclei rise in the epithelium and the level of aop rises dramatically. In pupal eye discs, aop protein is expressed in cone cells, in pigment cells, and in one cell of the bristle group.
GBrowse - Visual display of RNA-Seq signalsView Dmel\aop 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.
aop is dispensible for primary tracheal branching, but plays a key role in tracheal tip cell fate specification, where it acts to inhibit both terminal cell and fusion cell specification, by inhibiting MAPK and Wingless signaling respectively.
dsRNA has been made from templates generated with primers directed against this gene. RNAi of aop results in increased arborization of ddaD and ddaE neurons. RNAi also causes defects in muscle, alterations in the number of MD neurons, defects in dendrite morphogenesis and reproducible defects in da dendrite development.
SL2 cells transfected with dsRNA made from templates generated with primers directed against this gene show decreased levels of endocytosis.
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.
260 enhancers and 90 suppressors have been identified in a screen for genes functioning downstream in the Ras/MAPK/yan pathway, by virtue of interacting with alleles of aop.
Genetic studies suggest that 14-3-3ε functions in multiple receptor tyrosine kinase pathways, acting downstream or parallel to phl, but upstream of aop and phyl, two nuclear factors involved in Ras85D signalling.
Mutant phenotype indicates both aop and ttk are involved in the Ras/MAPK pathway, although their mechanisms of action to inhibit to inhibit cell fate might be different. aop and ttk synergistically interact in an inhibitory signaling pathway that is critical for neural cell fate determination.
Transcription factors Jra and aop are required for dorsal closure. Results suggest that the bsk pathway governs dorsal closure at least partially by regulating dpp expression via phosphorylation of Jra and aop.
pros gene becomes transcriptionally activated at a low level in all sev-competent cells prior to sev signaling and this requires the activities of Ras85D and two ETS transcription factors, aop and pnt.
Map kinase mediated down-regulation of aop function appears to be critical for the proper differentiation of both neuronal and nonneuronal tissues throughout development. This suggests that aop is an essential component of a general timing mechanism controlling the competence of a cell to respond to inductive signals.
Phosphorylation of aop by rl map kinase affects the stability and subcellular localisation of aop resulting in rapid down regulation of aop activity. Expression of mutant aop in Schneider S2 cells demonstrates that the first phosphorylation site is absolutely required in the response to activation of the Ras85D/rl pathway, phosphorylation at other sites is important for modulation or amplification of the response.
aop has a role in the specification of the fate of the cell that develops into R7 from the true R7 precursor. Mosaic analysis suggests the function of the aop gene product is autonomously required for the development of a cell as a photoreceptor neuron. The complete loss of aop during development does not give rise to an adult retina with extra photoreceptor neurons.
aop functions as a cell-autonomous negative regulator of photoreceptor development. In the presumptive R7 and cone cells aop appears to act synergistically to the proneural signal mediated by sev and Ras85D.
Mosaic analysis demonstrates that no photoreceptor cell absolutely requires aop for proper ommatidial development.