Glued, Gl, p150Glued, p150, dynactin
Please see the GBrowse view of Dmel\DCTN1-p150 or the JBrowse view of Dmel\DCTN1-p150 for information on other features
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Low-frequency RNA-Seq exon junction(s) not annotated.
Annotated transcripts do not represent all supported alternative splices within 5' UTR.
Gene model reviewed during 5.46
4.6 (compiled cDNA)
5.5 (northern blot)
There is only one protein coding transcript and one polypeptide associated with this gene
135/150 (kD observed)
145/160 (kD observed)
1319 (aa); 148 (kD predicted)
Large macromolecular complex of at least 10 components; p150(glued) binds directly to microtubules and to cytoplasmic dynein.
Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\DCTN1-p150 using the Feature Mapper tool.
Gl transcript is detected throughout embryonic development. It is also detected in the head, ovary, and testis of adult flies.
Gl transcript is expressed at high levels in embryos, but expression decreases in first and second instar larvae. Expression levels increase once more in third instar larvae and pupae. Gl is also expressed in unfertilized eggs. By in situ hybridization, Gl is detected in all embryonic, late larval and pupal tissues.
During early oogenesis, Gl protein is distributed throughout all cells in the anterior germarium. It subsequently accumulates in the 1 cell destined to be the oocyte in germarium region 2b. At stage S9, it localizes to the posterior pole of the oocyte. Gl protein distribution is indistinguishable from that of cytoplasmic dynein. When immunolocalization is performed in a background mutant for cytoplasmic dynein, Gl protein mislocalizes with cytoplasmic dynein.
GBrowse - Visual display of RNA-Seq signals
View Dmel\DCTN1-p150 in GBrowse 23-41
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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.
polyclonal
Source for identity of: Gl CG9206
Source for identity of: DCTN1-p150 Gl
RNAi screen using dsRNA made from templates generated with primers directed against this gene causes spindle pole detachment when assayed in S2 cells. This phenotype can be observed when the screen is performed with or without Cdc27 dsRNA.
dsRNA made from templates generated with primers directed against this gene tested in RNAi screen for effects on Kc167 and S2R+ cell morphology.
The Gl product has a role in assembling both the chemical and electrical components of the giant fiber synapse, suggesting that retrograde signalling may be essential for synapse formation and maturation.
Mutations in Gl disrupt fast organelle transport in both directions in axons.
After reaching the CNS, mutant axons exhibit errors in branching within the target domain.
Gl, a component of the dynein-dynactin complex, appears to have a role in normal terminal branching, synaptogenesis and stabilisation of some sensory neurons.
Mutation of Gl causes defects in mitosis, nuclear migration, cell fate determination, rhabdomere morphogenesis and cell death.
Mutants alter the anatomy of axons of the femoral chordotonal organ and disrupt the resistance reflex between the sensory neurons of the chordotonal organ and the tibial extensor motor neurons. Disruption of the dynein-dynactin complex disrupts sensory axon path finding during metamorphosis, and this in turn disrupts synaptic connectivity.
17 EMS-induced lethal mutants are lethal in combination with either Gl1 or Df(3L)Gl2 and appear to be point mutations, since they complement lethals in flanking loci. The time of death varies. Approximately one-fourth (22/96) revertants of Gl induced by X or γ irradiation fail to complement one or more flanking lethals and are therefore presumed to be deficiencies; those induced by EMS and hybrid dysgenesis on the other hand complement all flanking lethals. Phenotypic revertants induced by ionizing radiation and EMS remain lethal in heterozygous combination with either Gl or Df(3L)Gl2 and with each other; revertants tested in combination with Df(3L)Gl2 die during the first larval instar. The majority of hybrid-dysgenesis-induced revertants (67/78) are viable in heterozygous combination with Df(3L)Gl2 and most "Gll" alleles, whereas they are lethal in combination with Gl1, Gll9, and Gll10; 7/67 are viable in all the above combinations and 4/67 are inviable in all combinations.
Mutant alleles showed no interaction with mw2.
Adult eye is rough with irregular facets, rhabdomere number per ommatidia is irregular and eye disc cluster pattern is irregular.
Somatic-crossover studies and temperature-shift experiments with Glrv50, a temperature-sensitive allele, suggest that Gl+ gene product is required in mid-third instar; abnormal retinula fiber projections first observed in late third instar. Bristles generally shortened slightly and straighter than normal. Viability and fertility of heterozygote good.
Architecture of the optic ganglia severely deranged; attributable to the mutant genotype of the overlying eye tissue.
