A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\rhove-1

General Information
SymbolDmel\rhove-1SpeciesD. melanogaster
NameFlyBase IDFBal0017855
Feature typealleleAssociated geneDmel\rho
Also Known Asrhove, ve1, rhove1
Allele classloss of function allele
Mutagenspontaneous
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Description
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FB2013_03
Stocks
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
Mutation within the promoter region.
Carried on aberration
Cytology
hide Phenotypic Data
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hide Phenotype Manifest In
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Statement
Reference
Homozygous rho[ve-1] flies exhibit truncated wing veins.
Homozygotes lack the distal portion of wing vein L3 and lack most of the L4 and L5 wing veins.
Homozygous rho[ve-1] mutants show loss of partial L3, L4 and L5 and weakened L2-L4 M veins, whereas heterozygous rho[ve-1] exhibit only a weakened distal portion of L5 vein.
rhove-1 flies show a partial loss of wing veins L3, L4 and L5.
The initial development of most veins in the wing is disrupted in rhove-1 mutants.
rhove-1 mutants are viable, exhibiting partial loss of L3-L5 wing veins.
Homozygotes show incomplete wing veins L2, L3, L4 and L5.
Mutant embryos show duplication of the segmental border muscle and a complete loss of lateral adult muscle precursors.
rhove-1 mutant flies show loss of the distal ends of wing veins, particularly L3, L4 and L5.
The interactions between rhove-1/rhove-1 and emcD or emc1/emc11 are additive. The interactions between rhove-1/rho9 and emcD or emc1/emc11 are additive. emc1 clones in rhove-1 vn1 wings differentiate as veins in positions possibly corresponding to those of wild-type veins. Vein differentiation in these clones frequently fails in distal regions of veins.
In a e1, rhove-1 double mutant, in which all of the longitudinal veins are truncated or eliminated, ectopic melanin only develops in proximal areas that truncate before reaching the margin.
Germline clones fail to rescue the female sterile phenotype of Fs(3)Apc.
Homozygotes lack the distal ends of all longitudinal wing veins.
Wings lack the longitudinal veins.
rhove-1 supresses the vein defects of bs mutations although L2 to L5 remain truncated distally.
Wings have shortened longitudinal veins that do not reach the wing margin.
Lack distal segments of wing veins especially veins L4 and L5. Homozygous phenotype is strongly suppressed by heterozygous rhoWk.
Wing veins do not reach margins.
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hide Phenotypic Class
hideEnhanced by
Statement
Reference
rhove-1 has visible phenotype, enhanceable by aoshs.PSa
hideSuppressed by
Statement
Reference
rho9/rhove-1, vnM2/vn1 has visible phenotype, suppressible by bs03267/bs2
hideNOT suppressed by
Statement
Reference
rhove-1 has viable phenotype, non-suppressible by frcRY34/frc[+]
rhove-1 has visible phenotype, non-suppressible by Bap170hfl1/Bap170[+]
hideEnhancer of
Statement
Reference
rhove-1/rho[+] is an enhancer of size defective | adult stage phenotype of sl2
rhove-1/rho[+] is an enhancer of visible | dominant phenotype of sogEP7
rhove-1/rho[+] is an enhancer of visible | dominant phenotype of sogEP11
rhove-1 is an enhancer of visible phenotype of aoshs.PSa
hideSuppressor of
Statement
Reference
rhove-1/rho[+] is a suppressor of visible | heat sensitive phenotype of HC2.hs
rhove-1/rho[+] is a suppressor of visible | recessive phenotype of px1
hideOther
Statement
Reference
hide Phenotype Manifest In
hideEnhanced by
Statement
Reference
rhove-1 has wing vein L3 phenotype, enhanceable by Pc4
rhove-1 has wing vein L5 phenotype, enhanceable by brm2
rhove-1 has wing vein L5 phenotype, enhanceable by Df(2R)ED3921
rhove-1 has wing vein phenotype, enhanceable by aoshs.PSa
rhove-1 has wing vein phenotype, enhanceable by Egfrt1/Egfrf1
hideNOT Enhanced by
Statement
Reference
rhove-1 has phenotype, non-enhanceable by astK6
rhove-1 has wing vein L3 phenotype, non-enhanceable by Df(2R)ED3921
rhove-1 has wing vein L4 phenotype, non-enhanceable by Df(2R)ED3921
hideSuppressed by
Statement
Reference
brm2, rhove-1 has wing vein L5 phenotype, suppressible by Snr1E1
Df(3L)ru-22/rhove-1 has wing vein L5 phenotype, suppressible by Rab52
Df(3L)ru-22/rhove-1 has wing vein L5 phenotype, suppressible by shrbG5
rho9/rhove-1, vnM2/vn1 has wing vein phenotype, suppressible by bs03267/bs2
rhove-1 has phenotype, suppressible by bsPx
rhove-1 has phenotype, suppressible by gra1
rhove-1 has wing vein L2 phenotype, suppressible by kst1
rhove-1 has wing vein L3 phenotype, suppressible by kst1
rhove-1 has wing vein L4 phenotype, suppressible by kst1
rhove-1 has wing vein L5 phenotype, suppressible | partially by Eps-15e75
rhove-1 has wing vein L5 phenotype, suppressible | partially by Hrsv28
rhove-1 has wing vein L5 phenotype, suppressible | partially by kst1
rhove-1 has wing vein L5 phenotype, suppressible | partially by Rbsn-540-3
rhove-1 has wing vein L5 phenotype, suppressible | partially by shrbG5
rhove-1 has wing vein L5 phenotype, suppressible by Rab52
rhove-1 has wing vein L5 phenotype, suppressible by Snr1R3/Snr1E1
rhove-1 has wing vein L5 phenotype, suppressible by Vps20I3
rhove-1 has wing vein L5 phenotype, suppressible by Vps25A3
rhove-1 has wing vein L5 phenotype, suppressible by Vps28B9
rhove-1 has wing vein phenotype, suppressible by bs2
rhove-1 has wing vein phenotype, suppressible by bs11
rhove-1 has wing vein phenotype, suppressible by bsba
hideNOT suppressed by
Statement
Reference
rhove-1 has wing vein L3 | distal phenotype, non-suppressible by Bap170hfl1/Bap170[+]
rhove-1 has wing vein L3 phenotype, non-suppressible by frcRY34/frc[+]
rhove-1 has wing vein L4 phenotype, non-suppressible by Bap170hfl1/Bap170[+]
rhove-1 has wing vein L4 phenotype, non-suppressible by frcRY34/frc[+]
rhove-1 has wing vein L5 phenotype, non-suppressible by Bap170hfl1/Bap170[+]
rhove-1 has wing vein L5 phenotype, non-suppressible by frcRY34/frc[+]
hideEnhancer of
Statement
Reference
rhove-1/rho[+] is an enhancer of wing blade phenotype of sl2
rhove-1/rho[+] is an enhancer of wing vein | ectopic phenotype of sl2
rhove-1/rho[+] is an enhancer of wing vein phenotype of sogEP7
rhove-1/rho[+] is an enhancer of wing vein phenotype of sogEP11
rhove-1 is an enhancer of wing vein phenotype of aoshs.PSa
hideNOT Enhancer of
Statement
Reference
rhove-1/vn1 is a non-enhancer of wing vein | ectopic phenotype of bwkΔ11, cicD49
rhove-1 is a non-enhancer of wing disc phenotype of ftk07918
hideSuppressor of
Statement
Reference
rhove-1/rho[+] is a suppressor of wing | heat sensitive phenotype of HC2.hs
rhove-1/rho[+] is a suppressor of wing phenotype of px1
rhove-1/rho[+] is a suppressor of wing vein | ectopic | heat sensitive phenotype of HC2.hs
rhove-1 is a suppressor of wing phenotype of bsA48
rhove-1 is a suppressor of wing vein | ectopic phenotype of bsA48
rhove-1 is a suppressor of wing vein phenotype of tkv1/tkv8
hideNOT Suppressor of
Statement
Reference
rhove-1/rhove-1 is a non-suppressor of wing & microchaeta | ectopic phenotype of HC2.Scer\UAS, Scer\GAL4en-e16E
rhove-1 is a non-suppressor of wing disc phenotype of ftk07918
hideOther
Statement
Reference
hide Additional Comments
hide Genetic Interactions
Statement
Reference
rho[ve-1], vn[1] double mutant wings retain wild-type hair polarity and ridge orientation. Wings of homozygous pk[30], rho[ve-1] and vn[1] triple mutant flies lack veins L2-5. Wing anterior hairs of these mutants consistently have a posterior component to their polarity and posterior hairs have an anterior component to their polarity.
One copy of rho[ve-1] enhances the reduction in wing blade area seen in homozygous sl[2] males. One copy of rho[ve-1] significantly enhances the ectopic wing vein phenotype seen in sl[2] homozygotes. One copy of rho[ve-1] partially suppresses the percentage of sl[2] mutant ommatidia that contain extra R7 photoreceptors. The number of R7 cells per ommatidium is also reduced.
Introduction of one copy of kst[1] into a homozygous rho[ve-1] background completely suppresses the wing vein defect for L2-L4 and partially suppresses the defects in L5. A kst[2] heterozygous background results in a similar, but milder suppression. A reduction in the level of AnnIX, through expression of AnnIX[dsRNA.Scer\UAS] in the wing blade, under the control of Scer\GAL4[Bx-MS1096], restores wing vein formation in a rho[ve-1] background. A Rab5[2] heterozygous background leads to full suppression of the L5 wing vein defect in rho[ve-1]/Df(3L)ru-22 kst[1] mutants and 90% suppression in rho[ve-1]/rho[ve-1] kst[1] flies. A Rbsn-5[40-3] heterozygous background leads to just under 40% suppression of the L5 wing vein defect in both rho[ve-1]/Df(3L)ru-22 kst[1] and rho[ve-1]/rho[ve-1] kst[1] flies. A Hrs[v28] heterozygous background leads to approximately 30% suppression of the L5 wing vein defect in both rho[ve-1]/Df(3L)ru-22 kst[1] and rho[ve-1]/rho[ve-1] kst[1] flies. An Eps-15[e75] heterozygous background leads to approximately 70% suppression of the L5 wing vein defect in both rho[ve-1]/Df(3L)ru-22 kst[1] and rho[ve-1]/rho[ve-1] kst[1] flies. A Vps28[B9] heterozygous background leads to approximately 90% suppression of the L5 wing vein defect in both rho[ve-1]/Df(3L)ru-22 kst[1] and rho[ve-1]/rho[ve-1] kst[1] flies. A Vps25[A3] heterozygous background leads to approximately 90% suppression of the L5 wing vein defect in rho[ve-1]/rho[ve-1] kst[1] flies. A Vps20[I3] heterozygous background leads to approximately 90% suppression of the L5 wing vein defect in rho[ve-1]/Df(3L)ru-22 kst[1] flies. A shrb[G5] heterozygous background leads to almost full suppression of the L5 wing vein defect in rho[ve-1]/Df(3L)ru-22 kst[1] mutants and 80% suppression in rho[ve-1]/rho[ve-1] kst[1] flies.
The loss of wing veins seen in rho[ve-1] homozygotes is not suppressed by Bap170[hfl1]/+.
Wing veins do not develop in rho[ve-1], vn[1] animals. Overexpression of osa[Scer\UAS.cCa] in the wing under the control of Scer\GAL4[salm-459.2] cannot induce vein formation in a rho[ve-1], vn[1] mutant background.
Expression of Ubqn[dsRNA.Ex2.Scer\UAS] by Scer\GAL4[e22c] in a heterozygous rho[ve-1] background leads to a normal anterior cross vein and partially restored posterior cross vein and L5 vein, while the distal portion of L4 and L3-4 M veins corresponding to the posterior portion of the wing remains weakened, compared with Ubqn[dsRNA.Ex2.Scer\UAS]; Scer\GAL4[e22c] single mutants.
Df(2R)ED3921; rhove-1 flies show an enhancement of L5 vein loss compared to rhove-1 flies single mutants and partial loss of L2, a phenotype not seen in rhove-1 flies. There is no significant enhancement of L4 and L3 loss.
The wings of rhove-1 vn1 double mutants examined at 19, 21 or 24 hours after pupariation (AP) lack most longitudinal veins, with only the most proximal vein tissue intact 19 and 21 hours AP.
rhove-1 double mutants, heterozygous for frcRY34 exhibit the same phenotype as rhove-1 mutants.
rho[ve-1] vn[1] double homozygotes lack wing veins. This phenotype is partially suppressed by ash2[S112411] /ash2[S112411]. The degree of suppression varies from development of L2 only to almost complete rescue, albeit with some abnormalities such as extra crossvein material or proximal fusions between L2 and L3 or L4 and L5. In 25% of cases, hollow, tube like wings are formed, probably due to detachment of dorsal and ventral layers.
brm2 enhances the loss of wing vein L5 seen in rhove-1 homozygotes. Snr1E1/Snr1R3 suppresses the loss of wing vein L5 seen in rhove-1 homozygotes and rhove-1 suppresses the Snr1E1/Snr1R3 extra wing vein phenotype. Snr1E1 suppresses the shortened L5 wing vein that results from the interaction between rhove-1 and brm2.
The addition of bwkΔ11 and vn1 fails to enhance the extra wing vein phenotype seen in cicD49/bwkΔ11 animals.
When Egfrf1/Egfrt1 flies are raised at the non-permissive temperature (29oC) in a rhove-1/rhove-1 background, there is an enhancement of the usual rhove-1 homozygous wing vein phenotype.
vn1 rhove-1 flies completely lack wing veins.
h1 rhove-1 / h1 rhove-1 flies have ectopic bristles running between longitudinal veins.
rhove-1/astK6 double heterozygotes do not have a visible phenotype. The phenotype of rhove-1 homozygotes is not dominantly altered by astK6.
rho9, vnM2/rhove-1, vn1 double mutants lack wing veins. bs03267/bs2; rho9, vnM2/rhove-1, vn1 triple mutants show an almost wild type wing vein pattern.
vn1 rhove-1 double homozygotes lack all longitudinal wing veins. Vein tissue differentiates in vn1 rhove-1 double homozygotes when dppScer\UAS.cSa is expressed in these flies using Scer\GAL4C-580. rhove-1 suppresses the differentiation of thicker veins seen in tkv1/tkv8 flies, and results in fewer veins in combination with either dpps4/dpps8 or tkv1/tkv8.
rhove-1 vn1 double mutant flies lack all the longitudinal veins and crossveins of the wing blade. Dorsal and ventral implants of rhove-1 vn1 imaginal disc tissue into wild-type imaginal discs fail to differentiate veins.
vn1 rhove-1 flies lack wing veins.
rhove-1 homozygotes which are also expressing argoshs.PSa (using heat pulses from the second and third larval instar to pupal stage) lack most of wing veins L2-L4 and the entire L5 vein is eliminated. The campaniform sensilla on vein L3 usually remain intact.
hide Xenogenetic Interactions
Statement
Reference
Moderate expression of Zzzz\lef[Scer\UAS.cGa] under the control of Scer\GAL4[Bx-MS1096] in rho[ve-1] heterozygotes results in wing vein loss, while moderate Zzzz\lef[Scer\UAS.cGa] expression (with Scer\GAL4[Bx-MS1096]) alone doesn't have this phenotype.
Loss of the distal tips of wing veins seen in rhove-1 mutant flies is suppressed by Pstu\aarAScer\UAS.cGa; Scer\GAL4Bx-MS1096.
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Comments
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Bloomington
Kyoto
106017
hide Notes on Origin
Discoverer
Duncan, Jan. 1934.
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hide Synonyms & Secondary IDs ( 11 )
Reported As
Symbol Synonym
rho-1veinlet
Name Synonym
rhomboidve
veinlet
Secondary FlyBase IDs
hide References ( 61 )
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hide Recent research papers ( 5 )
Ajuria et al., 2011, Development 138(5): 915--924
Capicua DNA-binding sites are general response elements for RTK signaling in Drosophila. [FBrf0212975]
Hogan et al., 2011, PLoS Genet. 7(2): e1001305
Two frizzled planar cell polarity signals in the Drosophila wing are differentially organized by the fat/dachsous pathway. [FBrf0213159]
Murillo-Maldonado et al., 2011, PLoS ONE 6(11): e28067
Insulin Receptor-Mediated Signaling via Phospholipase C-γ Regulates Growth and Differentiation in Drosophila. [FBrf0216849]
Pilgram et al., 2011, J. Neurosci. 31(2): 492--500
The RhoGAP crossveinless-c Interacts with Dystrophin and Is Required for Synaptic Homeostasis at the Drosophila Neuromuscular Junction. [FBrf0212767]
Tjota et al., 2011, J. Cell Sci. 124(17): 2914--2926
Annexin B9 binds to {beta}H-spectrin and is required for multivesicular body function in Drosophila. [FBrf0215049]
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