a member of a family of adaptor proteins - F-BAR/SH3 protein that regulates synapse growth - controls synapse morphology by interacting with Wasp - regulates actin dynamics - interacts with thickveins and the endocytic machinery to attenuate retrograde BMP signaling during synaptic growth
Please see the JBrowse view of Dmel\nwk 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 5.53
Gene model reviewed during 5.45
Annotated transcripts do not represent all possible combinations of alternative exons and/or alternative promoters.
More transcripts are likely to exist; FBrf0175021 postulates at least 12 transcripts.
Gene model reviewed during 5.40
Low-frequency RNA-Seq exon junction(s) not annotated.
Gene model reviewed during 5.55
Homodimer (Probable) (PubMed:27601635). Interacts (via SH3 domain 1) with WASp (PubMed:14980202, PubMed:18701694, PubMed:27601635). Interacts (via SH3 domain 1) with shi/dynamin (PubMed:18498733, PubMed:18701694). Interacts (via SH3 domain 2) with Dap160 (PubMed:18498733, PubMed:18701694, PubMed:26686642). Interacts (via F-BAR domain) with SH3PX1 (PubMed:26567222). Interacts (via SH3 domain 2) with Snx16 (PubMed:21464232). Identified in a complex with Syn and Syt1 (PubMed:29568072).
In the autoinhibited state, the SH3 domains are bound to the concave surface of the F-BAR domain and prevent promiscuous membrane binding.
Upon heterologous expression, the isolated F-BAR domain is localized at the cell membrane, and causes the formation of cellular protrusions (PubMed:23761074, PubMed:26686642). Contrary to F-BAR domains from other proteins, causes membrane flattening on giant unilamellar vesicles (in vitro) (PubMed:23761074, PubMed:26686642). Binds to membranes enriched in phosphatidylserine and phosphatidylinositides, such as phosphatidylinositol 3-phosphate, phosphatidylinositol 3,4-bisphosphate and phosphatidylinositol 4,5-bisphosphate (PubMed:23761074, PubMed:26686642, PubMed:27601635).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\nwk 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: NOT detected in muscle
JBrowse - Visual display of RNA-Seq signals
View Dmel\nwk in JBrowse3-28
3-21.9
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
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Shows particularly robust cycling of transcription in adult heads, as assessed by expression analysis using high density oligonucleotide arrays with probe generated during three 12-point time course experiments over the course of 6 days.
Source for merge of: nwk CG4641
Annotations CG4684 and CG4641 merged as CG43479 in release 5.40 of the genome annotation.
Merge supported by RNA-seq junction and RNA-seq expression data, and by data presented in FBrf0175021.
Source for identity of: nwk CG4684
The gene is named "nervous wreck" after the behaviour of mutant flies; while their movement and coordination appear normal at room temperature, at 38[o]C they readily lose coordination and undergo seizures followed by paralysis.