serine/threonine kinase - segment polarity gene - cytoplasmic component of Hedgehog signaling pathway - Phosphorylation of the atypical kinesin Costal2 by Fused induces the partial disassembly of the Smoothened-Fused-Costal2-Cubitus interruptus complex in Hedgehog signalling
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 5.51
Low-frequency RNA-Seq exon junction(s) not annotated.
There is only one protein coding transcript and one polypeptide associated with this gene
805 (aa); 90 (kD predicted)
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\fu using the Feature Mapper tool.
Transcript is detected starting in the midgermarium in cells corresponding to mature 16-cell germline-cysts and prefollicular and follicual cells. Transcript is detected in stage 2 and 3 egg chambers with both somatic and germline cell expression.
fu transcripts are most abundant in early embryos and adult females. They are also observed at low levels in larvae, pupae, and adult males. Transcripts are first detected by in situ hybridization at stage S8 of oogenesis in nurse cells and appear to flow in the oocyte as oogenesis proceeds. fu transcripts are uniformly distributed in preblastoderm embryos, are located in cortical cells at the cellular blastoderm stage, and are present in all germ layers at similar levels in germ band extended embryos. They are not detected after germ band retraction. In imaginal discs, fu transcripts are present in all cells but are more abundant in wing than in leg discs.
GBrowse - Visual display of RNA-Seq signalsView Dmel\fu 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.
Source for identity of: fu CG6551
No complementation observed in 120 heteroallelic combinations (Wurst and Hanratty, 1979).
smo protein promotes the relocalisation of fu protein from vesicles to the plasma membrane in response to hh signaling and reciprocally, fu protein controls the stability and phosphorylation of smo protein.
Identified as a component of the hh signalling pathway in a genome-wide RNAi screen. dsRNA made from templates generated with primers directed affects the extent of expression of a hh signaling reporter construct in Clone 8 cells.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
fu participates in to partially redundant pathways to regulate ci nuclear import; the kinase function plays a positive role by inhibiting Su(fu), and the regulatory domain plays a negative role in conjunction with cos.
Using the yeast two-hybrid method and an in vitro binding assay it is demonstrated that Su(fu), ci and fu can interact directly to form a trimolecular complex, with Su(fu) binding to both its partners simultaneously. In the absence of hh signalling results propose that Su(fu) inhibits ci by binding to it and that, upon reception of the hh signal, fu is activated and counteracts Su(fu), leading to the activation of ci.
hh elicits signal transduction via a complex that includes the products of the fu, ci and cos genes. The complex binds with high affinity to microtubules in the absence of hh protein, but not when hh is present. The complex may facilitate signalling from hh by governing access of the ci product to the nucleus.
Genetic and molecular analysis of both endogenous and in vitro induced fu mutant alleles has been performed to characterise the function of fu and to assess the role of the different fu protein domains.
fu protein is phosphorylated during embryogenesis as a result of hh activity. Results from cell culture studies suggest that fu and Pka-C1 function downstream of hh but in parallel pathways that eventually converge distal to fu.
DNA comparison of fu and Dvir\fu identifies regions conserved during evolution: the 268 amino acid kinase domain and a domain within the third exon. Stretches of conserved sequences are also observed in the 5' and 3' untranslated sequences.
Mutations at the fu locus result in morphological defects in the adult compound eye and mechano-sensory bristles. Genetic analysis reveals that sca enhances the fu phenotype suggesting a possible interaction between fu and sca.
Scer\GAL4 under the control of wg, en, h and prd driving the expression of fu genomic fragment downstream of a UAS element has been used to test phenotypic rescue of fu- embryos be localised fu expression.
Mutants display hyperplastic phenotype, tissue overgrowth in mitotic recombination clones and in the germline.
Segment polarity mutations cause stripes of abnormal patterning within sectors of the leg disc, which may be mediated by regional perturbations in growth.
Competence of cells to express wg is independent of their ability to receive the hh signal. wg activation requires the function of fu, this suggests that the putative hh signal is transduced by the serine/threonine kinase that fu encodes.
The structure of the fu transcription unit, its temporal and spatial expression are analysed.
Wing phenotype and maternally determined lethality of fu mutants suppressed by loss of function mutations at Su(fu).
Mutations in fu cause extra longitudinal or transverse veins with plexated vein phenotypes. kn, fu and shf act synergistically against Px, px, net, dsr and emc.
Molecular data suggests that fu encodes a putative Ser/Thr protein kinase.
The kn and fu loci belong to the knot phenotypic group within the 'excess-of-vein' mutant class. Mutants generate a medial shift in the position of the longitudinal veins, sensilla and chaetae. Double mutants are superadditive in vein pattern defects.
Role of fu in neurogenesis has been studied.
Genetic analysis of viable and lethal alleles of fu has been performed and demonstrates that zygotic expression of fu is required for normal metamorphosis, while maternal expression is necessary for a normal segmentation pattern.
DNA sequences thought to contain fu have been identified and injected into fu mutant embryos: partial rescue of the mutant phenotype was obtained.
Veins L3 and L4 fused from base to beyond anterior crossvein with elimination of anterior crossvein and first basal cell. L3 and L4 fused at tip; this fusion may reach back to basal cell. L3 may be thickened and branched to varying degrees; L4 may be partially or completely absent. Mosaic wings in which the posterior compartment is nearly entirely fu/fu may develop normally; alternatively, patches of + tissue in a fu wing may develop a fu phenotype (Fausto-Sterling, 1978). Wings usually extended; flightless owing to cuticle defect (Deak, 1976). Ocelli reduced or absent; bristles of ocellar region small or absent. Eyes small and slightly rough. Phototactic response normal (Benzer, 1967). Anterior scutellar bristles reduced in number and scutellum shortened. Female late to eclose and has decreased longevity. Ovaries histologically normal at eclosion but with half the normal number of ovarioles (Beatty, 1949); fecundity 4% normal. Developing egg chambers may fuse or become tumorous with age (King, Burnett, and Staley, 1957). All aspects of phenotype respond in a coordinated fashion to experimental manipulation (Wust and Hanratty, 1979). Proportion of tumorous egg chambers increases by 6% per day. Females raised at 18oC show only 10% the tumor development of those raised at 25oC. Tumor formation also enhanced by presence of YS (King, 1969). Ovarian effects in females carrying fu and a deficiency for fu <up>E.G. In(1)ClLy4R</up> are more extreme than those in fu homozygote (King, 1959). Alleles vary in strength; measures of ovarian tumor formation revealed that fu1 = fu14 > fu7 > fu13 > fu11 = fu12 (Smith and King, 1966). fu/fu ovaries transplanted into fu+ hosts develop autonomously in regard to fertility (Clancy and Beadle, 1937) (Sobels, 1950) and tumor formation (Smith, Bodenstein and King, 1965). The few normal-appearing eggs that are laid by fu/fu females produce adults only if they have been fertilized by fu+-bearing sperm (Lynch, 1919). Eggs fertilized by fu- or Y-bearing sperm, with rare exceptions (Counce, 1956), develop into embryos that become abnormal 5-5.5 hr after fertilization. Lethal embryos exhibit incompletely penetrant segment polarity defects in which the anterior denticle-belt-bearing half of each segment shows mirror-image duplication replacing the naked cuticle of the posterior half; more pronounced in thoracic segments; penetrance in right and left hemisegments at the same level is not necessarily correlated. (Nusslein-Volhard and Wieschaus, 1980; Gergen and Wieschaus, 1986). Elimination of regions of dorsal pattern and occasional head defects are also observed. fu eggs from fu/+ mothers develop normally. Segment polarity defects autonomous in mosaics (Gergen and Wieschaus, 1986). Heterozygous daughters from homozygous mothers on the other hand, often have abnormal abdominal segmentation and, as embryos, have abnormal musculature. This is a maternal effect not found in the reciprocal cross and it is temperature-sensitive (Armstrong and Sobels).
Bridges, 4th Nov. 1912.