S8, l(3)S8, shm
transcription factor - bHLH - pas homology - required for the developmental specification of the ventral midline
Please see the JBrowse view of Dmel\sim for information on other features
To submit a correction to a gene model please use the Contact FlyBase form
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.
673 (aa)
The carboxy-terminal half of the sim protein contains a number of alanine-alanine-glutamine repeats, a proline-rich region, and a glutamine-rich region.
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.
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: until 6h AEL. Assay specific to sim transcript sim-RA.
Comment: until 15h AEL. Assay specific to sim transcript sim-RB.
Comment: Assay specific to sim transcript sim-RB.
Comment: Assay specific to sim transcript sim-RB.
Comment: Assay specific to sim transcript sim-RB.
Comment: Assay specific to sim transcript sim-RB.
Comment: 24-48h APF. Assay specific to sim transcript sim-RB.
Comment: 72-96h APF. Assay specific to sim transcript sim-RB.
Comment: Assay specific to sim transcript sim-RB.
Comment: Assay specific to sim transcript sim-RB.
Comment: Assay specific to sim transcript sim-RB.
Comment: Assay specific to sim transcript sim-RB.
sim is expressed in the ventral regions of the embryonic foregut and hindgut.
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.
Comment: reference states 5 hr AEL
Comment: all cells
Comment: all cells
Comment: all cells
Comment: ubiquitous expression
GBrowse - Visual display of RNA-Seq signals
View Dmel\sim in GBrowse 23-53
Maps just distal to pic.
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.
sim is required for the association of lamina neurons with R axons.
ChEST reveals this is a target of Mef2.
Five EMS induced alleles were identified in a screen for mutations affecting commissure formation in the CNS of the embryo.
Expression of sim is required for the formation of the dorsal medial cells.
The PAS domain of sim confers its target gene specificity.
Dorsal median cells fail to form in sim mutants.
sim functions to repress ventral ectodermal cell fates.
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.
sim is a master regulator of mesectodermal cell differentiation.
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.
sim is required for the emergence of a specific subset of neuronal and nonneuronal precursor cells lying along the midline of the developing neuroepithelium.