S8, l(3)S8, shm
Gene model reviewed during 5.53
Gene model reviewed during 5.47
Gene model reviewed during 5.55
3.5, 3.0 (northern blot)
None of the polypeptides share 100% sequence identity.
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\sim using the Feature Mapper tool.
Expression assayed at stages 9, 11, 13, and 17. Expression may be continuous between assayed stages in some tissues.
sim is first detected in the mesoderm at stage 11 in a cluster of 3-5 cells per hemisegment lying just adjacent to the ventral midline. In late stage 11, a more laterally place cluster is observed. Shortly after their appearance, sim-expressing mesodermal cells migrate laterally away from the midline towards the body wall. By the beginning of germ band retraction, the two cell clusters merge and form a single row of sim-positive cells on either side of the ventral midline. These cells elongate and begin to take on the morphology of muscle syncytia. sim expression begins to fade shortly after muscle cell fusion. Weak staining can be detected later in a subset of ventral oblique muscles.
sim protein is first observed at the end of gastrulation in a strip of cells along the ventral midline. The sim-positive cells extend up into the presumptive head region where they form an annulus around the presumptive anterior midgut invagination. By hour 5, the neuroblasts begin delaminating from the ectodermal epithelium. sim-positive cells delaminate to give rise to the midline cells of the CNS. sim protein is expressed in precursors of both neuronal and non-neuronal cells lying at the midline but is found at different level in different cells. By later stages, expression is low in the median neuroblast and in the VUM neurons and is high in the six midline glial cells.
GBrowse - Visual display of RNA-Seq signalsView Dmel\sim 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.
N activity is required for sim expression in cellularising embryos. Su(H) activity is required to upregulate sim expression in the mesectoderm, and to prevent ectopic expression of sim dorsally in the neurectoderm in cellularising embryos.
Five EMS induced alleles were identified in a screen for mutations affecting commissure formation in the CNS of the embryo.
sim and trh activate transcription by forming dimers with the tgo protein. Gene dosage studies reveal in vivo interactions between sim and tgo, and trh and tgo. The interacting proteins in vivo control CNS midline and tracheal transcription and development.
Facilitating the expression of spi, rho and S is the only sim- dependent contribution of the midline to patterning the ventral ectoderm, since the mutant sim ectodermal defects can be overcome by expression of secreted spi in the ectoderm.
DNA binding coimmunoprecipitation assays studying the interaction of human Arnt with other PAS proteins demonstrates human Arnt forms heterodimers with per and sim, by means of the PAS domain, in a cooperative way.
Ectopic transplantations of wild-type midline cells into sim mutants suggest that the ventral midline is required for the correct positioning of the cells.
sim can function as a transcriptional activator. Three independent activation domains are identified in the carboxy terminal region that include areas rich in Ser, Thr, Gln and Pro. Germ line transformation experiments indicate that the carboxy terminal activation domains, the PAS dimerisation domain and the putative DNA binding basic domain of sim are required for expression of CNS midline genes in vivo.
Mutations of sim do not result in an absence of somatic muscles but a mislocalisation of ventral muscle precursor cells such that muscle fibres form across the inside of the embryo instead of along the body wall. Mutations that eliminate sim muscle precursor expression but leave CNS expression intact reveal no abnormalities in muscle formation. Thus the muscle defect results from a non-autonomous influence of the CNS on myogenesis.
Sequence analysis of sim, Tl and sli revealed a conserved sequence ACGTG that resembles the mammalian xenobiotic response element. This motif forms the core of an element required for CNS midline transcription.
Analysis of sim mutant embryos implies that ventral epidermal cell fate is influenced by the CNS midline cells.
sim gene product is required for the proper development of the ventralmost cuticle and the CNS midline.
Mutant analysis demonstrates that sim is required for the proper differentiation of the midline cells from their progenitors.