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General Information
Symbol
Dmel\Rho172O
Species
D. melanogaster
Name
FlyBase ID
FBal0061661
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
RhoA72O, Rho1720, rhoA720
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Imprecise excision of the P{lacW} element, deleting part of the coding region, including the translation start site.
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference
No myoblast fusion defects are observed in Rho172O zygotic mutants. Expression of Rho1N19.Scer\UAS in founder cells under the control of Scer\GAL4kirre-rP298 disrupts myoblast fusion in wild type embryos. A more severe phenotype is seen in Rho172O mutant embryos. In contrast to the round and dense morphology seen in wild type, the F-actin enriched-structures between unfused fusion-competent myoblasts and miniature myotubes in Rho172O mutant embryos expressing Rho1N19.Scer\UAS under the control of Scer\GAL4kirre-rP298 are irregularly shaped and exhibit abnormally long invasive protrusions. Ribosomes and intracellular organelles are frequently observed within the abnormal protrusions. Fusion pores fail to form.
Zygotic mutant embryos show head defects and excess naked cuticle replacing the ventral denticles.
Mutant embryos have holes in the head cuticle.
Rho172F/Rho172O stage 16 embryos have longer dorsal trunks than normal.
F-actin localisation at the level of the adherens junctions is disrupted in Rho172O homozygous clones.
Homozygotes are embryonic lethal, and often have a hole in the head cuticle.
The shape of the invaginated mesoderm is abnormal in embryos with a reduced maternal dose of Rho1+.
Homozygous embryos show defects in head involution and organisation of the leading edge at stage 14. At stage 15, puckering of the leading edge is seen.
Rho172O/Rho172R embryos exhibit dramatic defects in head involution. None of these mutant embryos have a clear dorsal hole, although they frequently show puckering or segment misalignments along the closed midline seam. During dorsal closure lamellipodial and filopodial protrusions are more abundant at the leading edge than in wild-type, significantly increaing the total protrusive area of the leading edge. The cytoskeletal architecture typical of the leading edge is lost.
Laser wounded Rho172R/Rho172O embryos fail to assemble a continuous actin cable in wound-edge cells and there is little or no initial contraction of the leading edge of these cells. The leading-edge extends filopodia that are longer (extending up to 12 μm) and approximately three times more common than in wild-type embryos. In many instances, several filopodia coalesce to form a lamellipodium. Lamellipodia from adjacent leading-edge cells apparently tug on one another, resulting in the formation of several local zipping fronts around the wound margin, a behaviour only observed in wild-type in the last moments of wound closure, when opposing epithelial fronts are driven close enough together. Despite these differences with the wild-type, Rho172R/Rho172O embryos are able to close their wounds, but these take on average almost twice as long to repair as in their wild-type counterparts. There is a lag phase of nearly 2 hours (the time in which an equivalent wild-type wound can close fully) before the disorganized leading edge begins to move forward significantly. During this initial period, no obvious changes in cell shape occur in the leading-edge epithelial cells. However, once forward movement begins, the wound closes at a rate that is not significantly different to that of a wild-type wound (7.0+/-1.9 μm2/min; n = 6 in the mutant compared with 9.0+/-2.6 μm2/min; n = 5 in the wild type).
Homozygous clones in the mushroom body result in a reduction in the number of neurons produced by the clone and the presence of multinucleated cells.
Rho1E3.10/Rho172O embryos have dorsal anterior holes in their cuticle. The embryos have compacted posterior spiracles.
Homozygous mushroom body neuroblast clones in larvae cease division within 24 hours after clone induction, in contrast to wild-type clones. 63%, 57% or 29% of larvae contain one homozygous Rho172O mushroom body neuroblast clone when examined at 36, 18 or 16 hours after heat shock induction of mitotic recombination (which produces the homozygous clone), respectively. This indicates that in the majority of the clones, the last mitosis, which gives rise to two large nuclei (which are characteristic of these clones), has occurred by 18 hours after heat shock. However, BrdU incorporation is still occurring at 18-24 hours after heat shock in all cases, indicating that there is at lease one additional round of DNA replication after the last mitosis in the majority of homozygous clones. The two large nuclei are always present in the same cell body and in addition, one or two cell bodies are found to contain two small nuclei in each homozygous clone. This suggests a cytokinesis defect. Each large nucleus in the clone contains on average 3.30 +/- 0.38-fold more DNA compared with a diploid nucleus. The multinuclear cells containing the large nuclei appear to acquire a differentiated neuronal fate. Neuronal processes are occasionally seen projecting from these cells. Neurons of two cell or single cell mushroom body neuroblast clones homozygous for Rho172O and generated in newly hatched larvae have axon projections that are indistinguishable from wild type. The number of major and minor branches within the adult γ lobe is not significantly different from wild type. Homozygous Rho172O mushroom body neuroblast clones show a striking overextension of their dendrites. The length, frequency and number of overextended dendrites is drastically increased compared to wild-type clones.
Homozygotes show a defect in dorsal closure.
In homozygous mutant embryos, cytokinesis is blocked in affected cells. Many cells in the head region of the embryo become polyploid and contain two nuclei per cell. In addition polyploid cells are occasionally found in thoracic or abdominal segments of mutant embryos. Homozygous mutants have an "anterior open" phenotype.
Rho172F/Rho172O, Rho172F/Rho172R and Rho172R/Rho172O embryos have an "anterior open" phenotype; the epidermis fails to close in the dorsal/anterior region. Rarely, the dorsal epidermis also fails to close. Some head structures are missing.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT Enhanced by
Statement
Reference
Suppressed by
Statement
Reference
Rho172O, zipEbr has visible | dominant phenotype, suppressible | partially by Mbs3
Enhancer of
Statement
Reference
Rho172O/Rho1[+] is an enhancer of visible phenotype of Drakdel
Rho172O/Rho1[+] is an enhancer of visible phenotype of DrakKO
Rho172O/Rho1[+] is an enhancer of neuroanatomy defective phenotype of p120ctn308
Rho172O/Rho1[+] is an enhancer of visible phenotype of Scer\GAL4hs.PB, towUAS.cCa
Rho172O/Rho1[+] is an enhancer of visible phenotype of CycEJP
Rho172O/Rho1[+] is an enhancer of visible | dominant phenotype of Sb70
Rho172O/Rho1[+] is an enhancer of visible | dominant phenotype of br1
Rho172O/Rho1[+] is an enhancer of visible | dominant phenotype of Sb63b
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
Rho172O/Rho1[+] is a suppressor | partially of lethal | recessive phenotype of CG1093906373
Rho172O/Rho1[+] is a suppressor of visible phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E
Rho172O/Rho1[+] is a suppressor | partially of neuroanatomy defective | somatic clone phenotype of ssh1-11
Rho172O/Rho1[+] is a suppressor | partially of visible | heat sensitive phenotype of Sbhs.PB
Rho172O/Rho1[+] is a suppressor of visible | heat sensitive phenotype of fzI.hs
NOT Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
NOT Enhanced by
Statement
Reference
Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference
Rho172O is an enhancer of myoblast phenotype of kirrerP298-G4
Rho172O is an enhancer of myoblast phenotype of Ced-1250
Rho172O/Rho1[+] is an enhancer of wing phenotype of Drakdel
Rho172O/Rho1[+] is an enhancer of wing phenotype of DrakKO
Rho172O/Rho1[+] is an enhancer of embryonic/larval cuticle phenotype of baz4
Rho172O/Rho1[+] is an enhancer of embryonic/larval cuticle phenotype of bazG0484
Rho172O/Rho1[+] is an enhancer of wing hair | supernumerary phenotype of Scer\GAL4hs.PB, towUAS.cCa
Rho172O/Rho1[+] is an enhancer of eye phenotype of CycEJP
Rho172O/Rho1[+] is an enhancer of leg phenotype of Sb70
Rho172O/Rho1[+] is an enhancer of leg phenotype of br1
Rho172O/Rho1[+] is an enhancer of leg phenotype of Sb63b
Rho172O/Rho1[+] is an enhancer of eye & ommatidium phenotype of tumdsRNA.UAS.cBa, Scer\GAL4ey.PB
NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference
Rho172O/Rho1[+] is a suppressor of embryo | embryonic stage 5 phenotype of stepSH0323/stepk08110
Rho172O/Rho1[+] is a suppressor of furrow canal phenotype of stepSH0323/stepk08110
Rho172O/Rho1[+] is a suppressor | partially of crossvein phenotype of Scer\GAL4en-e16E, Rokcat.UAS
Rho172O/Rho1[+] is a suppressor of zonula adherens & disc epithelium proper phenotype of CskdsRNA.UAS, Scer\GAL4ptc-559.1
Rho172O/Rho1[+] is a suppressor of wing phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E
Rho172O/Rho1[+] is a suppressor | partially of adult mushroom body | somatic clone phenotype of ssh1-11
Rho172O/Rho1[+] is a suppressor | partially of leg | heat sensitive phenotype of Sbhs.PB
Rho172O is a suppressor | partially of ommatidium phenotype of pkpk.sev
Rho172O/Rho1[+] is a suppressor | partially of eye phenotype of Rac1GMR.PN
Rho172O/Rho1[+] is a suppressor of wing hair | supernumerary phenotype of fzI.hs
NOT Suppressor of
Statement
Reference
Rho172O/Rho1[+] is a non-suppressor of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053
Rho172O is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, pksple.UAS
Rho172O is a non-suppressor of ommatidium phenotype of Scer\GAL4sev.PM181, stanUAS.cUa
Rho172O is a non-suppressor of eye phenotype of Pp2B-14Dact.GMR
Rho172O is a non-suppressor of eye phenotype of CanBGMR.PS, Pp2B-14Dact.GMR
Rho172O is a non-suppressor of ommatidium phenotype of Scer\GAL4hs.2sev, msnEP549
Other
Additional Comments
Genetic Interactions
Statement
Reference
Rho172O Rok2 double zygotic mutants exhibit myoblast fusion defects. In contrast to the round and dense morphology seen in wild type, the F-actin enriched-structures between unfused fusion-competent myoblasts and miniature myotubes are irregularly shaped and exhibit abnormally long protrusions. Expression of sqhE21.T:Zzzz\FLAG suppresses the myoblast fusion defect seen in Rho172O Rok2 double mutant embryos. Expression of sqhA20.A21.T:Zzzz\FLAG does not suppress the myoblast fusion defect seen in Rho172O Rok2 double mutant embryos. Rho172O enhances the myoblast fusion defects seen in kirrerP298 mutant embryos. Expression of sqhE21.T:Zzzz\FLAG partially suppresses the myoblast fusion defects seen in kirrerP298 Rho172O mutant embryos, returning fusion to the level of kirrerP298 mutants alone. Rho172O enhances the myoblast fusion defects seen in Ced-1250 mutant embryos. Expression of Rho1Scer\UAS.P\T.T:Avic\GFP in founder cells under the control of Scer\GAL4kirre-rP298 partially suppresses the myoblast fusion defects seen in Ced-1250 Rho172O mutant embryos, returning fusion to the level of Ced-1250 mutants alone. No suppression is seen when Rho1Scer\UAS.P\T.T:Avic\GFP is expressed in fusion-competent myoblasts under the control of Scer\GAL4sns.PK. Expression of FimScer\UAS.T:Avic\GFP-YFP.Venus significantly rescues the myoblast fusion defects seen in Rho172O mutant embryos expressing Rho1N19.Scer\UAS in founder cells under the control of Scer\GAL4kirre-rP298.
Maternal heterozygosity for Rho172O substantially suppresses the abnormal perpendicular membrane expansion seen at the base of cellularization furrows in embryos derived from females expressing sstndsRNA.shRNA.Scer\UAS.P\T.2 under the simultaneous control of Scer\GAL4otu.T:Hsim\VP16, Scer\GAL4nos.PG and Scer\GAL4nos.UTR.T:Hsim\VP16.
Maternal heterozygosity for Rho172O almost completely suppresses the furrow canal expansion phenotype seen in embryos derived from mothers expressing stepHMS00365 under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16. The number of endocytic tubules emanating from furrow canals during early cellularisation is restored. Maternal heterozygosity for Rho172O almost completely suppresses the furrow canal expansion phenotype seen in stepSH0323/stepk08110 mutant embryos.
An average of 27.8 +/- 5% of Sip106373/Sip106373 ; Rho172O/+ animals survive to adulthood.
Rho172O dominantly enhances the shortening of the wing which is seen in DrakKO and in Drakdel flies.
The cuticle phenotype of dead embryos derived from baz4/+ embryos derived from a cross of baz4/+ females to wild-type males is enhanced if the females also carry one copy of Rho172O. The cuticle phenotype of dead embryos derived from bazG0484/+ embryos derived from a cross of bazG0484/+ females to wild-type males is enhanced if the females also carry one copy of Rho172O.
The Rho172O/+ heterozygous mutation can partially suppress the GluRIIASP16 NMJ synaptic homeostatic response. The ExnEY01953/+ heterozygous mutation does not enhance the Rho172O/+, GluRIIASP16 double mutant NMJ synaptic homeostasis phenotype. The combination of Rho172O/+ and cacS/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIASP16 genetic background.
Rho172O clones expressing diaCA.Scer\UAS.T:Ivir\HA1 still exhibit disrupted adherens junctions. Expression of Rab11S25N.Scer\UAS.P\T.T:Avic\GFP-YFP in Rho172O clones enhances the Rho1 mutant phenotype. In addition to frequent disruptions to adherens junctions between clonal cells, there is also disruption of adherens junctions between clonal and wild-type cells. Cdc42dsRNA.Scer\UAS expression suppresses the adherens junctions defects observed between two Rho172O cells but does not suppress the increased apical area. Expression of Rab5S43N.Scer\UAS.P\T.T:Avic\GFP-YFP in Rho172O clones suppresses the adherens junction defect seen between two Rho172O cells, although decreased apical tension is not affected. Expression of Rab5Q88L.Scer\UAS.P\T.T:Avic\GFP-YFP (under the control of Scer\GAL4Act5C.PI) in Rho172O clones does not worsen the Rho172O adherens junction phenotype between two clonal pigment epithelial cells but does disrupt adherens junctions between a pigment epithelial cell and cone cell, a phenotype that is not found in Rho172O clones. Expression of Rab5GD10492 in Rho172O clones suppresses the adherens junction defect seen between two Rho172O cells, although decreased apical tension is not affected. Expression of Rab11S25N.Scer\UAS.P\T.T:Avic\GFP-YFP in Rho172O clones enhances the Rho1 mutant phenotype. In addition to frequent disruptions to adherens junctions between clonal cells, there is also disruption of adherens junctions between clonal and wild-type cells.
dia2 homozygotes in which maternal Rho1 function is reduced (derived from Rho172O heterozygous females) nearly all die as embryos, with defects in head involution, ventral cuticle or the completion of dorsal closure. Maternal heterozygosity for dia2 enhances the dia2 homozygous phenotype, resulting in ventral holes in the cuticle. 13% of the progeny of dia2 Rho172O double heterozygous females die as embryos, largely with defects in head involution. These embryos show dramatic alterations in amnioserosal cell behaviour compared to wild type; during germband retraction, amnioserosal cells along all the germband of the mutant embryos form long persistant cell extensions extending over neighbouring epidermal cells. The protrusions are especially prominent caudally, but are also observed laterally and anteriorly. Long protrusions are occasionally seen from epidermal cells and amnioserosal cells also extend abnormal processes over one another as well as over epidermal cells. Dorsal closure in these embryos is otherwise normal, except that drop-out cells appear much earlier in dorsal closure than normal.
Rho172O dominantly enhances the recessive p120ctn308 supernumerary tertiary pigment cell phenotype and increases the frequency of the inter-ommatidial cell patterning errors in the pupal retina.
The multiple wing hair phenotype caused by expression of towScer\UAS.cCa under the control of Scer\GAL4hs.PB using heat shock at 24 hours after puparium formation is enhanced if the flies are also carrying one copy of Rho172O.
Rho172O/+ partially suppresses the wing phenotype of animals expressing rokcat.Scer\UAS under the control of Scer\GAL4en-e16E.
Rho172O/+ suppresses the loss of apical profile, delamination and subsequent migration and cell death increase seen in cells at the posterior edge of the ptc expression domain in CskIR.Scer\UAS Scer\GAL4ptc-559.1 third instar larvae.
Rho172O/+ suppresses the mutant wing phenotype caused by expression of LIMK1Scer\UAS.cCa under the control of Scer\GAL4en-e16E (the % of wings with normal morphology at 18oC is increased from 9% to 97%). The frequency of the malformed leg phenotype seen in Sb63b/+ heterozygotes (8%) is increased if the flies are also heterozygous for Rho172O (31%). The frequency of the malformed leg phenotype seen in Sb70/+ heterozygotes (7%) is increased if the flies are also heterozygous for Rho172O (56%). The frequency of the malformed leg phenotype seen in br1/Y males (1%) is increased if the flies are also heterozygous for Rho172O (12%).
The stidsRNA.Sym.Scer\UAS Scer\GAL4ey.PB rough eye phenotype is significantly enhanced by Rho172O. The rough eye phenotype associated with the expression of RacGAP50CdsRNA.Scer\UAS, under the regulation of Scer\GAL4ey.PB in the developing eye imaginal disc is dominantly enhanced by Rho172O.
Rho172O shows a strong interaction (at least 50% of double heterozygotes have at least one malformed leg) with the following mutations: Sb63b and Sb70. The frequency of malformed legs seen in animals in which Sbhs.PB is expressed in a wild-type background using a 1 hour 37o heat shock in staged 0 hour or 3 hour prepupae is partially suppressed by Rho172O/+.
The small, rough eye phenotype of Rac1GMR.PN flies is partially suppressed by heterozygosity for Rho172O.
The proportion of symmetrical (R3/R3) ommatidia in the eyes of stanScer\UAS.cUa; Scer\GAL4sev.PM181 flies is unaffected by heterozygosity for Rho172O.
92% of Rho172O/zipEbr double heterozygotes have a malformed leg phenotype. 16% of Rho172O/Df(2R)Jp1 double heterozygotes show a malformed phenotype.
Has no effect on the ommatidial polarity phenoptype seen in flies with msnEP549 driven by Scer\GAL4hs.2sev.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Rho172O clones are rescued by expression of Rho1Scer\UAS.cMa. In some cases, a decrease in the apical area is observed, perhaps due to the high level of Rho1Scer\UAS.cMa overexpression.
Rho1Scer\UAS.cMa rescues the dendrite phenotype of homozygous Rho172O mushroom body neuroblast clones when expressed under the control of Scer\GAL4Tab2-201Y, without altering the proliferation defect.
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Mutant
Wild-type
Stocks (1)
Notes on Origin
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External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (11)
References (48)