Gene model reviewed during 5.47
None of the polypeptides share 100% sequence identity.
332 (aa); 36 (kD predicted)
Efficient DNA binding requires dimerization with another bHLH protein.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\nau using the Feature Mapper tool.
nau protein is first detected at embryonic stage 11 by immunolocalization. In each segment, clusters of nuclei on either side of the midline and a smaller lateral cluster are stained. Another small cluster appears later in a dorsal position in the segments from the labium to A7. During stage 11, the number of nau-expressing cells increases 2-3 fold to a total of 30-40 per hemisegment. Differences in the number and pattern of stained cells between the abdominal and more anterior segments are observed. As dorsal closure begins, the level of staining decreases rapidly. Only the nuclei of some muscle precursors and some clusters in the head continue to show high levels of nau protein. After dorsal closure, weak staining is seen in a variety of muscles. Stronger staining persists in the pharyngeal muscles and in muscles of the anterior spiracles and telson.
GBrowse - Visual display of RNA-Seq signalsView Dmel\nau 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.
Embryos lacking both maternal and zygotic nau function lack a distinct set of muscle fibres. This muscle loss is tolerated, however, such that the loss of both maternal and zygotic nau function does not result in lethality at any stage of development.
nau is not required for the formation of muscle precursors, but rather plays a role in the differentiation of a subset of muscle precursors into mature muscle fibres in the developing embryo.
Abnormalities in clusters of nau-producing cells appear in the neurogenic mutants, E(spl), N, Dl, bib, neu, mam, and amx, nau and βTub85D, during stage 11, the time of first detectable nau expression. The clusters arise at the correct developmental time and position but contain more cells than wild type clusters. This causes strong ectodermal abnormalities and has effects on mesoderm development.
Ecol\lacZ reporter gene constructs have demonstrated that the nau gene product is a transiently expressed nuclear protein that serves as a marker for myogenic precursor cells, or a subset of them, in development. These cells may represent muscle founder cells that are crucial in organising and establishing the precise muscle pattern in each segment of the body plan. nau is a distinctive gene and is not a member of a multigene family.
Isolated from a genomic library at low stringency using a mouse MyoD and rat myogenin probe.