l(2)br7, SuH, Supressor of Hairless, CSL, l(2)35Bh
transcription factor - integrase domain - Notch pathway - Notch intracellular domain associates with Su(H) and Mastermind, a transcriptional coactivator - operates as molecular switch on Notch target genes: within activator complexes, including intracellular Notch, or within repressor complexes, including the antagonist Hairless
Gene model reviewed during 5.52
Gene model reviewed during 5.57
Interacts with activated cleaved Notch. Interacts with Hairless, this interaction preventing its DNA-binding activity. Interacts with insv (via BEN domain).
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\Su(H) using the Feature Mapper tool.
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as ventral imaginal precursor specific anlage
Comment: reported as dorsal/lateral sensory complexes
Comment: reference states 16-24 hr APF
Su(H) is stronglyly detected in all macrochaete socket cells 17, 21 and 30 hours APF. It is also observed in microchaetes at these stages.
Su(H)@ transcripts are detected throughout development by RNAase protection.
Su(H) transcripts are present throughout the syncytial embryo. During cellularization, the rapid disappearance of putative maternal transcripts reveals a transient striped pattern. Transcripts are next observed from stage 11 on in external sensory organs. In the thoracic and abdominal segments the es cells were identified as the tormogen and trichogen. In late third instar larvae, expression is observed in many larval and imaginal tissues but not in the CNS. Transcripts are broadly distributed in the discs but in a nonuniform pattern. In the wing disc, transcripts are most abundant in the posterior region of the wing pouch. In the leg disc, expression is also observed in a posterior zone of the disc. In the eye-antennal disc, low levels of expression are observed posterior to the morphogenetic furrow and and in the central antennal region while higher levels are observed in the vicinity of the furrow and along the margins of the disc. In 16-24hr pupae, Su(H) is expressed in many tissues including developing muscle and epidermis. In michrochaetae and macrochaetae, expression is observed in a couple of large cells that appear to be the tormogen and trichogen. Expression in the tormogen occurs at a higher level.
Su(H) protein is observed in the nucleus in all cells in the third instar wing disc. It was sometimes observed in the surrounding cytoplasm of both macrochaete and microchaete SOPs. It is observed in the nucleus and cytoplasm of socket cells. It does not co-localize with N protein at the apicolateral membrane in socket cells.
Su(H) protein is strongly expressed in prohemocytes in the medullary zone of the lymph gland and is weakly expressed in differentiated hemocytes in the cortical zone.
Su(H) protein isdetected by western blots in extracts from embryos, third instar wingdiscs, and nota dissected from 24hr APF pupae. It\'s expression was studiedduring SOP specification by immunolocalization. In wing discs of latethird instar larvae, it is expressed at a low level in all nuclei. It ispresent equally in macrochaete SOPs and the neighboring proneuralclusters. A similar observation was made fro microchaete SOPs in thedeveloping notum at 14hr APF. In this case, Su(H) protein is detected inboth the microchaete SOPs and the surrounding epithelial cells. FollowingSOP division, no difference in staining is seen between SOPIIa and SOPIIb.With further differentiation of SOPIIa and SOPIIb, Su(H) proteinexpression is observed specifically in the socket cell. This is true insocket cells of the machrochaetes, microchaetes and the interommatidialbristle. Su(H) protein is also expressed in a small number of embryonicsense organ cells per segment. These support cells show a \'socket-like\'morphology.
GBrowse - Visual display of RNA-Seq signalsView Dmel\Su(H) 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.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
Su(H) has three distinct functions in the development of external mechanosensory organs; N-dependent transcriptional activation, an auto-repression function, both of which direct cell fate decisions, and an auto-activation function required for normal socket cell differentiation.
During wing development Su(H) can activate the expression of some N target genes independently of N. Activation of other N target genes depends on the joint activity of Su(H) and the intracellular fragment of the N protein; without the N fragment Su(H) acts as a repressor of these genes. Su(H) activity is inhibited by H, suggesting that the activation of Su(H) by N involves the release of Su(H) from an inhibitory complex which contains H.
Su(H) is essential to determine outer but not inner cell fates in the sensory organ cell lineage.
N is processed in a ligand-dependent manner to generate a phosphorylated cytoplasmic domain that preferentially associates with Su(H). Localization studies suggest that the relative levels of Su(H), Dl and N regulate nuclear entry of the N/Su(H) complex.
Mutants isolated in a screen of the second chromosome identifying genes affecting disc morphology.
Factors, in addition to Su(H), must exist to confer tissue-specific expression of vg and to regulate the spatial and temporal features of vg expression within the wing pouch. Su(H) has differential roles in the dorsal and ventral wing boundary cells. Su(H) represses the vg quadrant enhancer at the D/V boundary.
Su(H) is required for only a subset of the asymmetric divisions that depend on the function of numb and N. Su(H) appears to act downstream of numb in the same genetic pathway in determining the fates of the IIa daughter cells, the hair cell and the socket cell, and Su(H) is negatively regulated by numb.
The genes of the E(spl) complex mediate only a subset of N activities during imaginal development. Comparisons of mutant phenotypes suggests that the N pathway bifurcates after the activation of Su(H) and that E(spl) activity is not required when the consequence of N function is the transcriptional activation of downstream genes. Transcriptional activation mediated by Su(H) and transcriptional repression mediated by E(spl) could provide greater diversity in the response of individual genes to N activity.
The proximal upstream region of E(spl) complex genes contains multiple specific binding sites for Su(H). Integrity of these sites and Su(H) activity are required not only for normal levels of E(spl) complex gene expression in imaginal disc proneural clusters but also for their transcriptional response to hyperactivity of the N receptor. Su(H) is a direct regulatory link between N receptor activity and the expression of E(spl) complex genes, extending the known lineage of the N cell-cell signaling pathway.
There is a strict genetic requirement for Su(H) activity for cell fate choices during early neurogenesis.
Glutathione-S-transferase (GST) fusion proteins and the yeast two hybrid system demonstrate the H protein can inhibit the in vitro DNA binding activity of Su(H) through direct protein-protein interactions. Co-transfection assays in S2 cells demonstrate transcriptional activation driven by Su(H) is also inhibited by H.
The dx gene product regulates the subcellular localisation of a transcription factor, Su(H), via antagonistic interactions with the N ankyrin repeats.
Notum cells require Su(H) activity for receiving the lateral inhibitory signal. The DNA binding protein encoded by the Su(H) gene may act downstream of the N receptor to implement the epidermal non-sense organ precursor (SOP) fate.
Yeast two-hybrid system assays and in vitro interaction studies demonstrate the sub-transmembrane region of N, structurally equivalent to the amino terminal part of mRAM23, is involved in the interaction with Su(H).
In vitro binding assays demonstrate the H gene product can inhibit the DNA binding of Su(H) through direct protein-protein interactions. Consistent with this, transcriptional activation driven by Su(H) in transfected S2 cells is inhibited by H. These results support a model in which H acts, in part, as a negative regulator of Su(H) activity.
The sequence similarity between Su(H) and the integrase domain is not of functional significance as Tyr315 is not required for gene function in vivo.
Isolated from a genomic library using the murine RBP-JΚ cDNA as a probe, under low stringency conditions.
Homozygous lethal; hemizygotes die in the pupal stage, between head eversion and the beginning of eye pigmentation. Heterozygotes in the absence of H are wild type in phenotype. Suppresses H; Su(H)/+; H/+ have 7-10 more bristles that H/+ alone; besides affecting the bristle phenotype of H, all alleles tend to enhance its wing-vein phenotype of shortening L4 and L5. Su(H) is without effect on the lethal phenotype of homozygous H. One homozygous-lethal allele acts as a dominant enhancer of H. Most alleles are amorphic or hypomorphic; heterozygous deficiencies for the locus also suppress and duplications enhance H (Nash, 1970). Enhanced genotypes have 10-15 fewer bristles and a far more extreme loss of microchaetae on the thorax than their unenhanced counterparts. The number of bristles in H/+ flies is inversely related to the dose of Su(H)+, with the number of bristles varying from fewer than ten with four doses to approximately 35 with one dose. Some combinations of hypomorphic alleles produce occasional escapers; survivors have distinctive phenotypes, which are described under entries for specific alleles.