A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\gbbScer\UAS.cKa

General Information
SymbolDmel\gbbScer\UAS.cKaSpeciesD. melanogaster
NameSaccharomyces cerevisiae UAS construct a of KhalsaFlyBase IDFBal0092971
Feature typealleleAssociated geneDmel\gbb
Allele class
Mutagenin vitro construct - regulatory fusion
hide Recent Updates
Description
What does this section display?
This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms).
What does this section not display?
This section does not currently display links that were removed or gene model changes.
Update Feed
Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates Click here to see a list of all updates to this record from FB2010_08 and on.
hide Nature of the Allele
Allele class
Mutagen
Mutations Mapped to the Genome
Type
Location
Additional Notes
References
Associated Sequence Data
DDBJ /
EMBL /
GenBank
DNA sequence
Protein sequence
Name
 
UniProtKB/Swiss-Prot
UniProtKB/TrEMBL
Progenitor genotype
Nature of the lesion
Statement
Reference
Construct: A 1.6kb EcoRI fragment of a gbb cDNA (containing the entire open reading frame) is expressed under the control of Scer\UAS regulatory sequences.
Carried in construct
Cytology
hide Phenotypic Data
hide Phenotypic Class
hide Phenotype Manifest In
synapse & neuromuscular junction, with gbb2/gbb1
hide Detailed Description
Statement
Reference
Expression of gbb[Scer\UAS.cKa] under the control of Scer\GAL4[en.PU] from the onset of pupal development (the temperature sensitive allele Scer\GAL80[ts.αTub84B] is used to restrict the stage during which expression occurs) results in wing defects which are more prominent in the posterior half.
Expression of gbb[Scer\UAS.cKa] under the control of Scer\GAL4[A9] results in a variable wing phenotype, marked by ectopic vein material.
Larvae expressing gbb[Scer\UAS.cKa] under the control of Scer\GAL4[D42] display a 40% increase in the number of boutons at neuromuscular junction (NMJ) 6/7 and a 62% increase in type I boutons at NMJ 4. Scer\GAL4[OK6]-mediated expression of gbb[Scer\UAS.cKa] has a comparable effect. Overexpression of gbb[Scer\UAS.cKa] using Scer\GAL4[A9] results in a severe wing blistering phenotype in 79% of females and a more severe phenotype, including unfurling and blistering of the wing in 93% of males.
Expression of gbb[Scer\UAS.cKa] under the control of Scer\GAL4[ptc-559.1] results in an ectopic wing vein phenotype.
Expression of gbb[Scer\UAS.cKa] in the wing with Scer\GAL4[ptc-559.1] induces an expanded region of ectopic vein where the anterior crossvein would normally form.
Overexpression of gbb[Scer\UAS.cKa] post-synaptically under the control of Scer\GAL4[eve.RN2] increases synaptic current amplitude compared to controls.
Expression of gbbScer\UAS.cKa in the wing disc at 25oC, under the control of Scer\GAL4A9, produces wings divided into four classes of phenotypic severity according to the amount of extra wing vein material present in the wing.
The proximal 25% of the anterior margin of a gbbScer\UAS.cKa/Scer\GAL4ap-md544 wing has no bristles. More distally, the triple row reappears but is quite irregular. When gbbScer\UAS.cKa is driven in all the cells of the wing blade with Scer\GAL4C-765, the phenotype is similar but less severe.
Overexpression of gbbScer\UAS.cKa, under the regulation of Scer\GAL4A9, can result in wing disruption.
Postsynaptic expression of gbbScer\UAS.cKa, under the control of Scer\GAL4eve.RN2, results in the averaged amplitude of synaptic currents recorded from whole-cell voltage clamp recordings of aCC/RP2 motoneurons being significantly increased compared with controls. In contrast, expression of gbbScer\UAS.cKa in presynaptic cholinergic interneurons, driven by Scer\GAL4B19, does not affect the averaged synaptic current amplitude.
gbbScer\UAS.cKa; Scer\GAL4C587 females do not have increased numbers of germ-line stem cells in their germaria.
Expression of gbbScer\UAS.cKa under the control of Scer\GAL4A9 produces slightly broadened wings consisting of solid veins.
Expression of gbbScer\UAS.cKa under the control of Scer\GAL4dpp.blk1 does not produce a mutant phenotype. Expression of gbbScer\UAS.cKa under the control of Scer\GAL4en-e16E results in overgrowth of the wing disc and defects restricted to the posterior compartment of the wing.
Flies expressing gbbScer\UAS.cKa under the control of Scer\GAL4ptc-559.1 show ectopic vein material anterior to the anterior/posterior boundary in the wing, associated with a decrease in intervein tissue between veins L3 and L4. Flies expressing gbbScer\UAS.cKa under the control of Scer\GAL471B have wing blisters and ectopic vein material. Flies expressing gbbScer\UAS.cKa under the control of Scer\GAL4A9 show excessive vein formation in the wing.
hide External Data
Linkouts
hide Interactions
hide Phenotypic Class
hideEnhanced by
Statement
Reference
Scer\GAL4A9, gbbScer\UAS.cKa has visible phenotype, enhanceable by sax4/sax[+]
hideNOT Enhanced by
Statement
Reference
hideSuppressed by
Statement
Reference
Scer\GAL4A9, gbbScer\UAS.cKa has visible phenotype, suppressible | partially by tkv7/tkv[+]
Scer\GAL4A9, gbbScer\UAS.cKa has visible phenotype, suppressible by Mad12/Mad[+]
Scer\GAL4A9, gbbScer\UAS.cKa has visible phenotype, suppressible by Med[+]/Med1
Scer\GAL4A9, gbbScer\UAS.cKa has visible phenotype, suppressible by put[+]/put135
Scer\GAL4A9, gbbScer\UAS.cKa has visible phenotype, suppressible by shn3.3/shn[+]
Scer\GAL4A9, gbbScer\UAS.cKa has visible phenotype, suppressible by tkv5/tkv[+]
Scer\GAL4A9, gbbScer\UAS.cKa has visible phenotype, suppressible by tkv8/tkv[+]
hideNOT suppressed by
Statement
Reference
hideSuppressor of
Statement
Reference
hideNOT Suppressor of
Statement
Reference
gbbScer\UAS.cKa/Scer\GAL4eve.RN2 is a non-suppressor of neurophysiology defective | heat sensitive phenotype of Chats2
hideOther
Statement
Reference
hide Phenotype Manifest In
hideEnhanced by
Statement
Reference
Scer\GAL4A9, gbbScer\UAS.cKa has wing vein phenotype, enhanceable by sax4/sax[+]
hideNOT Enhanced by
Statement
Reference
hideSuppressed by
Statement
Reference
Scer\GAL4A9, gbbScer\UAS.cKa has wing vein phenotype, suppressible by Mad12/Mad[+]
Scer\GAL4A9, gbbScer\UAS.cKa has wing vein phenotype, suppressible by Med[+]/Med1
Scer\GAL4A9, gbbScer\UAS.cKa has wing vein phenotype, suppressible by put[+]/put135
Scer\GAL4A9, gbbScer\UAS.cKa has wing vein phenotype, suppressible by shn3.3/shn[+]
Scer\GAL4A9, gbbScer\UAS.cKa has wing vein phenotype, suppressible by tkv5/tkv[+]
Scer\GAL4A9, gbbScer\UAS.cKa has wing vein phenotype, suppressible by tkv8/tkv[+]
hideNOT suppressed by
Statement
Reference
hideSuppressor of
Statement
Reference
hideOther
Statement
Reference
hide Additional Comments
hide Genetic Interactions
Statement
Reference
The severity of the wing phenotype caused by expression of gbb[Scer\UAS.cKa] under the control of Scer\GAL4[A9] is reduced by co-expression of sax[Scer\UAS.T:Zzzz\FLAG].
Co-expression of cmpy[Scer\UAS.cJa] suppresses the neuromuscular overgrowth phenotype caused by expression of gbb[Scer\UAS.cKa] using either Scer\GAL4[D42] or Scer\GAL4[OK6]. Co-expression of cmpy[Scer\UAS.cJa] suppresses the wing blistering phenotype caused by Scer\GAL4[A9]-mediated expression of gbb[Scer\UAS.cKa] in males and females.
Mesodermal expression of gbb[Scer\UAS.cKa] (under the control of Scer\GAL4[how-24B]) suppresses the phenotype observed with frac[Scer\UAS.cMa] over-expression (48% to 28%).
Co-expression of either sog[Scer\UAS.cYa] or Hip14[Scer\UAS.cKa] suppresses the ectopic wing vein phenotype caused by expression of gbb[Scer\UAS.cKa] under the control of Scer\GAL4[ptc-559.1].
Overexression of gbb[Scer\UAS.cKa] with Ppt1[Scer\UAS.cKa], both under the control of Scer\GAL4[GMR.PF] suppresses the visual system degeneration seen upon Ppt1[Scer\UAS.cKa] expression alone.
The ectopic vein phenotype in the area where the anterior crossvein normally forms resulting from the Scer\GAL4[ptc-559.1] driven expression of gbb[Scer\UAS.cKa] can be suppressed by co-expressing kek5[Scer\UAS.T:Avic\GFP] in the wing. The ectopic vein phenotype in the area where the anterior crossvein normally forms resulting from the Scer\GAL4[ptc-559.1] driven expression of gbb[Scer\UAS.cKa] is not influenced by co-expressing kek4[Scer\UAS.T:Avic\GFP] in the wing.
Overexpression of gbb[Scer\UAS.cKa] post-synaptically under the control of Scer\GAL4[eve.RN2] fails to suppress the reduced synaptic currents found in Cha[ts2] mutant second instar larvae raised at 18[o]C.
Expression of cv-2[Scer\UAS.cSa] suppresses the wing phenotypes seen when gbb[Scer\UAS.cKa] is expressed under the control of Scer\GAL4[A9].
Coexpression of gbbScer\UAS.cKa in the wing disc with saxScer\UAS.T:Ivir\HA1, under the control of Scer\GAL4A9, results in an enhancement of the Scer\GAL4A9>gbbScer\UAS.cKa wing vein phenotype; all wings show the mildest form of vein phenotype in the gbbScer\UAS.cKa-saxScer\UAS.T:Ivir\HA1 coexpressing wings, while less than 10% of wings show this mild phenotype in gbbScer\UAS.cKa wings. Expression of gbbScer\UAS.cKa, under the control of Scer\GAL4A9, in a sax4/+ background partially suppresses the extra wing vein phenotype; over 90% of flies expressing both UAS transgenes show the most severe form of the Scer\GAL4A9>gbbScer\UAS.cKa phenotype, compared to about 20% of Scer\GAL4A9>gbbScer\UAS.cKa flies. Coexpression of tkvScer\UAS.T:Ivir\HA1 and gbbScer\UAS.cKa enhances the Scer\GAL4A9>gbbScer\UAS.cKa wing vein phenotype so that a higher percentage of wings have extensive amounts of wing vein tissue. Expression of gbbScer\UAS.cKa, under the control of Scer\GAL4A9, in a tkv7/+ background suppresses the extra wing vein phenotype of Scer\GAL4A9>gbbScer\UAS.cKa flies. Around 80% of Scer\GAL4A9>gbbScer\UAS.cKa; tkv7/+ wings show a very mild vein phenotype, while around 20% appear wild type.
Co-expression of cvScer\UAS.cVa with gbbScer\UAS.cKa, under the regulation of Scer\GAL4A9 has no detectable effect on the overexpression phenotype of gbbScer\UAS.cKa (wing disruption). Co-expression of cvScer\UAS.cVa and sogScer\UAS.cYa, with gbbScer\UAS.cKa, under the regulation of Scer\GAL4A9 re-establishes the intervein tissue and the longitudinal veins with a series of expanded crossveins between L2 and L3 on the wing. Therefore, cv and sog interact together to suppress the wing phenotype of gbb. Co-expression of tsgScer\UAS.cYa and sogScer\UAS.cYa, along with gbbScer\UAS.cKa, under the regulation of Scer\GAL4A9 partially suppresses the excess gbbScer\UAS.cKa wing disruption phenotype. Co-expression of tsgScer\UAS.cYa and gbbScer\UAS.cKa, under the regulation of Scer\GAL4A9 suppresses the excess gbb phenotype.
Postsynaptic expression of gbbScer\UAS.cKa, under the control of Scer\GAL4eve.RN2, fails to potentiate synaptic current amplitude in aCC/RP2 neurons when expressed in a Chats2 homozygous background at 29oC, compared to in a Chats2/+ control background. If larvae are allowed to recover at 20oC for another 22 hours, the ability of gbbScer\UAS.cKa to potentiate synaptic current amplitude in a Chats2 background is restored.
The solid vein phenotype caused by expression of gbbScer\UAS.cKa under the control of Scer\GAL4A9 is strongly suppressed by co-expression of sogScer\UAS.cYa or of sogsupersog1.Scer\UAS.
Flies expressing gbbScer\UAS.cKa under the control of Scer\GAL4A9 at 25oC have slightly larger wings than normal with minor venation defects along veins L2 and L5. Flies expressing gbbScer\UAS.cKa under the control of Scer\GAL4A9 at 30oC have blistered and highly pigmented wings. The wing phenotype caused by expression of gbbScer\UAS.cKa under the control of Scer\GAL4A9 is partially suppressed if the flies are also coexpressing tkv1ΔGSK.Scer\UAS, and is almost completely suppressed if the flies are also coexpressing saxΔI.Scer\UAS.
hide Xenogenetic Interactions
Statement
Reference
The wing phenotype caused by expression of gbb[Scer\UAS.cKa] under the control of Scer\GAL4[A9] is suppressed by co-expression of Hsap\ACVR1[Scer\UAS.T:Zzzz\FLAG] and the resulting flies have a reduction in wing size and a loss of wing vein material.
The solid vein phenotype caused by expression of gbbScer\UAS.cKa under the control of Scer\GAL4A9 is not suppressed by co-expression of Xlae\nogginScer\UAS.cYa.
hide Complementation & Rescue Data
Rescues
Partially rescues
gbbScer\UAS.cKa/Scer\GAL4[-] partially rescues gbb2/gbb1
Comments
The phenotypes associated with homozygous gbb[1] mutants (including lethality, larval transparency and abnormal fatty acid uptake and transport to the fat body) are rescued by expression of gbb[Scer\UAS.cKa] driven by Scer\GAL4[fat].
The presence of P{UAS-gbb.K}9.9 alone (in the absence of any driver) can rescue survival of gbb1/gbb2 animals to 3rd instar or pupal stage. The additional presence of Scer\GAL4G14 rescues bouton density and spontaneous mini-EJP (excitatory junctional potential) frequency to wild-type levels, and partially rescues spontaneous mini-EJP amplitude, evoked EJP frequency and levels of neurotransmitter release at synapses. Essentially identical results are seen when Scer\GAL4BG380 is used instead (although bouton density not measured). However, when Scer\GAL4elav-C155 is used there is only a slight rescue of bouton density, but the frequency and amplitude of spontaneous mini-EJPs, the amplitude of evoked EJPs and the levels of neurotransmitter release at synapses are all rescued to wild-type levels.
The testis defects seen in gbb4 homozygous males are rescued by expression of gbbScer\UAS.cKa under the control of Scer\GAL4nos.UTR.T:Hsim\VP16.
hide Stocks ( 0 )
hide Notes on Origin
Discoverer
hide External Crossreferences & Linkouts
Other Crossreferences
Linkouts
hide Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym
gbbScer\UAS.cKa
 
gbbUAS.cKa
 
Name Synonym
Saccharomyces cerevisiae UAS construct a of Khalsa
Secondary FlyBase IDs
hide References ( 28 )
Generate a list of
List References by type
hide Recent research papers ( 4 )
Fritsch et al., 2012, J. Biol. Chem. 287(8): 5942--5953
Different Requirements for Proteolytic Processing of Bone Morphogenetic Protein 5/6/7/8 Ligands in Drosophila melanogaster. [FBrf0217533]
Le and Wharton, 2012, Dev. Dyn. 241(1): 200--214
Hyperactive BMP signaling induced by ALK2(R206H) requires type II receptor function in a Drosophila model for classic fibrodysplasia ossificans progressiva. [FBrf0217004]
James and Broihier, 2011, Development 138(15): 3273--3286
Crimpy inhibits the BMP homolog Gbb in motoneurons to enable proper growth control at the Drosophila neuromuscular junction. [FBrf0214390]
Miller et al., 2011, J. Neurosci. 31(14): 5335--5347
Drosophila mmp2 regulates the matrix molecule faulty attraction (frac) to promote motor axon targeting in Drosophila. [FBrf0213409]