FlyBase Allele Report: Dmel\Rho1[72O]

General Information

Symbol

Dmel\Rho1^72O

Species

D. melanogaster

Name

FlyBase ID

FBal0061661

Feature type

allele

Associated gene

Dmel\Rho1

Associated Insertion(s)

Carried in Construct

Also Known As

RhoA^72O, Rho1⁷²⁰, rhoA⁷²⁰

Key Links

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Strutt et al., 1997)

Progenitor genotype

Rho1^k07236

(Strutt et al., 1997)

Cytology

Description

Imprecise excision of the P{lacW} element, deleting part of the coding region, including the translation start site.

(Strutt et al., 1997)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

abdominal ventral denticle belt

(Greer et al., 2013)

adherens junction | somatic clone

(Warner and Longmore, 2009)

adult mushroom body | somatic clone

(Billuart et al., 2001)

dendrite | larval stage | somatic clone

(Lee et al., 2000)

embryo

(Prokopenko et al., 1999)

embryo | dorsal closure stage

(Bloor and Kiehart, 2002, Lu and Settleman, 1999)

embryonic/first instar larval cuticle

(Homem and Peifer, 2008)

embryonic/first instar larval cuticle | anterior | dorsal (with Rho1^E3.10)

(Halsell et al., 2000)

embryonic/larval cuticle

(Shao et al., 2010)

embryonic/larval cuticle | ventral

(Greer et al., 2013)

embryonic/larval posterior spiracle (with Rho1^E3.10)

(Halsell et al., 2000)

embryonic/larval tracheal dorsal trunk (with Rho1^72F)

(Chung et al., 2009)

embryonic dorsal epidermis

(Strutt et al., 1997)

embryonic dorsal epidermis | anterior

(Prokopenko et al., 1999, Strutt et al., 1997)

embryonic epidermis | dorsal

(Lu and Settleman, 1999)

embryonic head

(Greer et al., 2013, Homem and Peifer, 2008)

embryonic head (with Rho1^72R)

(Jacinto et al., 2002)

embryonic leading edge cell

(Bloor and Kiehart, 2002)

embryonic leading edge cell (with Rho1^72R)

(Jacinto et al., 2002)

filopodium (with Rho1^72R)

(Jacinto et al., 2002)

head

(Strutt et al., 1997)

mushroom body & dendrite | somatic clone

(Lee et al., 2000)

mushroom body & neuron | somatic clone

(Billuart et al., 2001, Lee et al., 2000)

myoblast, with Rho1^N19.UAS, Scer\GAL4^{kirre-rP298-G4}

(Kim et al., 2015)

Detailed Description

Statement

Reference

No myoblast fusion defects are observed in Rho1^72O zygotic mutants.

Expression of Rho1^N19.Scer\UAS in founder cells under the control of Scer\GAL4^kirre-rP298 disrupts myoblast fusion in wild type embryos. A more severe phenotype is seen in Rho1^72O 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 Rho1^72O mutant embryos expressing Rho1^N19.Scer\UAS under the control of Scer\GAL4^kirre-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.

(Kim et al., 2015)

Zygotic mutant embryos show head defects and excess naked cuticle replacing the ventral denticles.

(Greer et al., 2013)

Mutant embryos have holes in the head cuticle.

(Shao et al., 2010)

Rho1^72F/Rho1^72O stage 16 embryos have longer dorsal trunks than normal.

(Chung et al., 2009)

F-actin localisation at the level of the adherens junctions is disrupted in Rho1^72O homozygous clones.

(Warner and Longmore, 2009)

Homozygotes are embryonic lethal, and often have a hole in the head cuticle.

(Homem and Peifer, 2008)

The shape of the invaginated mesoderm is abnormal in embryos with a reduced maternal dose of Rho1⁺.

(Wilson et al., 2005)

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.

(Bloor and Kiehart, 2002)

Rho1^72O/Rho1^72R 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.

(Jacinto et al., 2002)

Laser wounded Rho1^72R/Rho1^72O 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, Rho1^72R/Rho1^72O 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).

(Wood et al., 2002)

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.

(Billuart et al., 2001)

Rho1^E3.10/Rho1^72O embryos have dorsal anterior holes in their cuticle. The embryos have compacted posterior spiracles.

(Halsell et al., 2000)

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 Rho1^72O 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 Rho1^72O 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 Rho1^72O 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.

(Lee et al., 2000)

Homozygotes show a defect in dorsal closure.

(Lu and Settleman, 1999)

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.

(Prokopenko et al., 1999)

Rho1^72F/Rho1^72O, Rho1^72F/Rho1^72R and Rho1^72R/Rho1^72O 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.

(Strutt et al., 1997)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

GluRIIA^SP16, Rho1^72O/Rho1[+] has abnormal neurophysiology | third instar larval stage | recessive phenotype, non-enhanceable by Exn^EY01953/Exn[+]

(Frank et al., 2009)

Suppressed by

Statement

Reference

Rho1^72O, zip^Ebr has visible | dominant phenotype, suppressible | partially by Mbs³

(Mizuno et al., 2002)

Enhancer of

Statement

Reference

Rho1^72O/Rho1[+] is an enhancer of visible phenotype of Drak^del

(Neubueser and Hipfner, 2010)

Rho1^72O/Rho1[+] is an enhancer of visible phenotype of Drak^KO

(Neubueser and Hipfner, 2010)

Rho1^72O/Rho1[+] is an enhancer of abnormal neuroanatomy phenotype of p120ctn³⁰⁸

(Larson et al., 2008)

Rho1^72O/Rho1[+] is an enhancer of visible phenotype of Scer\GAL4^hs.PB, tow^UAS.cCa

(Chung et al., 2007)

Rho1^72O/Rho1[+] is an enhancer of visible phenotype of CycE^JP

(Brumby et al., 2004)

Rho1^72O/Rho1[+] is an enhancer of visible | dominant phenotype of Sb⁷⁰

(Chen et al., 2004)

Rho1^72O/Rho1[+] is an enhancer of visible | dominant phenotype of br¹

(Chen et al., 2004)

Rho1^72O/Rho1[+] is an enhancer of visible | dominant phenotype of Sb^63b

(Chen et al., 2004)

Rho1^72O/Rho1[+] is an enhancer of abnormal neuroanatomy phenotype of Pak^UAS.Tag:MYC, Scer\GAL4^ey-OK107

(Ng and Luo, 2004)

Rho1^72O is an enhancer of abnormal cytokinesis phenotype of Scer\GAL4^Bx-MS1096, pbl^{ΔDH497-549.UAS}

(Echard and O'Farrell, 2003)

NOT Enhancer of

Statement

Reference

Rho1^72O/Rho1[+] is a non-enhancer of visible phenotype of Scer\GAL4^en-e16E, kermit^GS2053

(Djiane and Mlodzik, 2010)

Rho1^72O/Rho1[+] is a non-enhancer of partially lethal - majority die phenotype of slpr^BS06

(Polaski et al., 2006)

Rho1^72O is a non-enhancer of abnormal cell polarity phenotype of Scer\GAL4^hs.2sev, pk^sple.UAS

(Jenny et al., 2003)

Rho1^72O is a non-enhancer of visible phenotype of Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Rho1^72O is a non-enhancer of visible phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Rho1^72O is a non-enhancer of abnormal planar polarity phenotype of Scer\GAL4^hs.2sev, msn^EP549

(Paricio et al., 1999)

Suppressor of

Statement

Reference

Rho1^72O/Rho1[+] is a suppressor | partially of lethal | recessive phenotype of CG10939⁰⁶³⁷³

(Hughes et al., 2010)

Rho1^72O/Rho1[+] is a suppressor of increased cell death phenotype of Csk^RNAi.UAS, Scer\GAL4^ptc-559.1

(Vidal et al., 2006)

Rho1^72O/Rho1[+] is a suppressor of visible phenotype of LIMK1^UAS.cCa, Scer\GAL4^en-e16E

(Chen et al., 2004)

Rho1^72O/Rho1[+] is a suppressor of abnormal neuroanatomy | somatic clone phenotype of ssh^1-11

(Ng and Luo, 2004)

Rho1^72O/Rho1[+] is a suppressor of abnormal neuroanatomy phenotype of LIMK1^UAS.Tag:HA, Scer\GAL4^ey-OK107

(Ng and Luo, 2004)

Rho1^72O/Rho1[+] is a suppressor of visible | heat sensitive phenotype of Sb^hs.PB

(Bayer et al., 2003)

Rho1^72O is a suppressor of abnormal cell polarity phenotype of pk^pk.sev

(Jenny et al., 2003)

Rho1^72O/Rho1[+] is a suppressor of visible | heat sensitive phenotype of fz^I.hs

(Winter et al., 2001)

NOT Suppressor of

Statement

Reference

Rho1^72O/Rho1[+] is a non-suppressor of visible phenotype of Scer\GAL4^en-e16E, kermit^GS2053

(Djiane and Mlodzik, 2010)

Rho1^72O is a non-suppressor of abnormal cell polarity phenotype of Scer\GAL4^hs.2sev, pk^sple.UAS

(Jenny et al., 2003)

Rho1^72O is a non-suppressor of visible phenotype of Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Rho1^72O is a non-suppressor of visible phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Rho1^72O is a non-suppressor of abnormal planar polarity phenotype of Scer\GAL4^hs.2sev, msn^EP549

(Paricio et al., 1999)

Other

Statement

Reference

Rho1^72O, dsh¹ has visible | adult stage phenotype

(Mieszczanek et al., 2022)

Rho1^72O, dsh^ΔPDZ has visible | adult stage phenotype

(Mieszczanek et al., 2022)

GluRIIA^SP16, Rho1^72O/Rho1[+] has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

GluRIIA^SP16, Rho1^72O/Rho1[+], cac^S/cac[+] has abnormal neurophysiology | recessive | third instar larval stage phenotype

(Frank et al., 2009)

Rho1^72O/Rho1[+], dia² has lethal | embryonic stage phenotype

(Homem and Peifer, 2008)

Rho1^72O/Rho1[+], Sb^63b has visible | dominant phenotype

(Bayer et al., 2003)

Rho1^72O/Rho1[+], Sb⁷⁰ has visible | dominant phenotype

(Bayer et al., 2003)

Rho1^72O, Sb^63b/Sb[+] has visible phenotype

(Bayer et al., 2003)

Rho1^72O, Sb[+]/Sb⁷⁰ has visible phenotype

(Bayer et al., 2003)

Rho1^72O/Rho1[+], zip^Ebr has visible | dominant phenotype

(Mizuno et al., 2002)

Rho1^72O, zip^Ebr has visible | dominant phenotype

(Mizuno et al., 2002, Halsell et al., 2000)

Rho1^72O, zip[+]/zip^Ebr has visible | dominant phenotype

(Halsell et al., 2000)

Df(2R)Jp1/+, Rho1^72O has visible | dominant phenotype

(Halsell et al., 2000)

Phenotype Manifest In

Enhanced by

Statement

Reference

Rho1^72O has adherens junction | somatic clone phenotype, enhanceable by Rab11^{S25N.UASp.YFP}/Scer\GAL4^Act5C.PI

(Warner and Longmore, 2009)

Rho1^72O has embryonic/first instar larval cuticle phenotype, enhanceable by dia²/dia[+]

(Homem and Peifer, 2008)

NOT Enhanced by

Statement

Reference

GluRIIA^SP16, Rho1^72O/Rho1[+] has embryonic/larval neuromuscular junction phenotype, non-enhanceable by Exn^EY01953/Exn[+]

(Frank et al., 2009)

Suppressed by

Statement

Reference

Rho1^72O, Rok² has myoblast phenotype, suppressible by sqh^E21.Tag:FLAG

(Kim et al., 2015)

Rho1^72O, Rho1^N19.UAS, Scer\GAL4^{kirre-rP298-G4} has myoblast phenotype, suppressible | partially by Fim^UAS.Venus, Scer\GAL4^{kirre-rP298-G4}

(Kim et al., 2015)

Rho1^72O, kirre^rP298-G4 has myoblast phenotype, suppressible | partially by sqh^E21.Tag:FLAG

(Kim et al., 2015)

Ced-12⁵⁰, Rho1^72O has myoblast phenotype, suppressible by Rho1^UASp.GFP/Scer\GAL4^{kirre-rP298-G4}

(Kim et al., 2015)

Rho1^72O has adherens junction | somatic clone phenotype, suppressible by Scer\GAL4^Act5C.PI/Cdc42^RNAi.UAS

(Warner and Longmore, 2009)

Rho1^72O has adherens junction | somatic clone phenotype, suppressible by Scer\GAL4^Act5C.PI/Rab5^{S43N.UASp.YFP}

(Warner and Longmore, 2009)

Rho1^72O has adherens junction | somatic clone phenotype, suppressible by Rab5^GD10492/Scer\GAL4^Act5C.PI

(Warner and Longmore, 2009)

Rho1^72O/Rho1[+], dia² has amnioserosa | maternal effect phenotype, suppressible by Ggal\MLCK^ct.UAS/Scer\GAL4^e22c

(Homem and Peifer, 2008)

Rho1^72O, zip^Ebr has wing phenotype, suppressible | partially by Mbs³

(Mizuno et al., 2002)

NOT suppressed by

Statement

Reference

Rho1^72O, Rok² has myoblast phenotype, non-suppressible by sqh^{A20.A21.Tag:FLAG}

(Kim et al., 2015)

Ced-12⁵⁰, Rho1^72O has myoblast phenotype, non-suppressible by Rho1^UASp.GFP/Scer\GAL4^{kirre-rP298-G4}

(Kim et al., 2015)

Rho1^72O has adherens junction | somatic clone phenotype, non-suppressible by Scer\GAL4^Act5C.PI/dia^{CA.UAS.Tag:HA}

(Warner and Longmore, 2009)

Rho1^72O has adherens junction | somatic clone phenotype, non-suppressible by Scer\GAL4^Act5C.PI/Rab5^{Q88L.UASp.YFP}

(Warner and Longmore, 2009)

Enhancer of

Statement

Reference

Rho1^72O is an enhancer of myoblast phenotype of kirre^rP298-G4

(Kim et al., 2015)

Rho1^72O is an enhancer of myoblast phenotype of Ced-12⁵⁰

(Kim et al., 2015)

Rho1^72O/Rho1[+] is an enhancer of wing phenotype of Drak^del

(Neubueser and Hipfner, 2010)

Rho1^72O/Rho1[+] is an enhancer of wing phenotype of Drak^KO

(Neubueser and Hipfner, 2010)

Rho1^72O/Rho1[+] is an enhancer of embryonic/larval cuticle phenotype of baz⁴

(Shao et al., 2010)

Rho1^72O/Rho1[+] is an enhancer of embryonic/larval cuticle phenotype of baz^G0484

(Shao et al., 2010)

Rho1^72O/Rho1[+] is an enhancer of tertiary pigment cell | increased number phenotype of p120ctn³⁰⁸

(Larson et al., 2008)

Rho1^72O/Rho1[+] is an enhancer of wing hair | increased number phenotype of Scer\GAL4^hs.PB, tow^UAS.cCa

(Chung et al., 2007)

Rho1^72O/Rho1[+] is an enhancer of eye phenotype of CycE^JP

(Brumby et al., 2004)

Rho1^72O/Rho1[+] is an enhancer of leg phenotype of Sb⁷⁰

(Chen et al., 2004)

Rho1^72O/Rho1[+] is an enhancer of leg phenotype of br¹

(Chen et al., 2004)

Rho1^72O/Rho1[+] is an enhancer of leg phenotype of Sb^63b

(Chen et al., 2004)

Rho1^72O/Rho1[+] is an enhancer of eye phenotype of Scer\GAL4^ey.PB, sti^RNAi.Sym.UAS

(D'Avino et al., 2004)

Rho1^72O/Rho1[+] is an enhancer of ommatidium phenotype of Scer\GAL4^ey.PB, sti^RNAi.Sym.UAS

(D'Avino et al., 2004)

Rho1^72O/Rho1[+] is an enhancer of adult mushroom body phenotype of Pak^UAS.Tag:MYC, Scer\GAL4^ey-OK107

(Ng and Luo, 2004)

Rho1^72O is an enhancer of wing hair | increased number phenotype of Scer\GAL4^Bx-MS1096, pbl^{ΔDH497-549.UAS}

(Echard and O'Farrell, 2003)

NOT Enhancer of

Statement

Reference

Rho1^72O/Rho1[+] is a non-enhancer of wing hair phenotype of Scer\GAL4^en-e16E, kermit^GS2053

(Djiane and Mlodzik, 2010)

Rho1^72O is a non-enhancer of ommatidium phenotype of Scer\GAL4^hs.2sev, pk^sple.UAS

(Jenny et al., 2003)

Rho1^72O is a non-enhancer of ommatidium phenotype of Scer\GAL4^sev.PM181, stan^UAS.cUa

(Das et al., 2002)

Rho1^72O is a non-enhancer of photoreceptor cell R3 | ectopic phenotype of Scer\GAL4^sev.PM181, stan^UAS.cUa

(Das et al., 2002)

Rho1^72O is a non-enhancer of photoreceptor cell R4 phenotype of Scer\GAL4^sev.PM181, stan^UAS.cUa

(Das et al., 2002)

Rho1^72O is a non-enhancer of eye phenotype of Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Rho1^72O is a non-enhancer of eye phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Rho1^72O is a non-enhancer of ommatidium phenotype of Scer\GAL4^hs.2sev, msn^EP549

(Paricio et al., 1999)

Suppressor of

Statement

Reference

Rho1^72O/Rho1[+] is a suppressor | maternal effect of furrow canal | maternal effect phenotype of Scer\GAL4^{VP16.nanos.UTR}, Scer\GAL4^VP16.otu, Scer\GAL4^nanos.PG, sstn^RNAi.UASp.2

(Liu et al., 2015)

Rho1^72O/Rho1[+] is a suppressor of embryo | embryonic stage 5 phenotype of Scer\GAL4^{VP16.mat.αTub67C}, step^HMS00365

(Lee and Harris, 2013)

Rho1^72O/Rho1[+] is a suppressor of furrow canal phenotype of Scer\GAL4^{VP16.mat.αTub67C}, step^HMS00365

(Lee and Harris, 2013)

Rho1^72O/Rho1[+] is a suppressor of embryo | embryonic stage 5 phenotype of step^SH0323/step^k08110

(Lee and Harris, 2013)

Rho1^72O/Rho1[+] is a suppressor of furrow canal phenotype of step^SH0323/step^k08110

(Lee and Harris, 2013)

Rho1^72O/Rho1[+] is a suppressor | partially of crossvein phenotype of Rok^cat.UAS.cVa, Scer\GAL4^en-e16E

(Verdier et al., 2006)

Rho1^72O/Rho1[+] is a suppressor of zonula adherens & disc epithelium proper phenotype of Csk^RNAi.UAS, Scer\GAL4^ptc-559.1

(Vidal et al., 2006)

Rho1^72O/Rho1[+] is a suppressor of wing phenotype of LIMK1^UAS.cCa, Scer\GAL4^en-e16E

(Chen et al., 2004)

Rho1^72O/Rho1[+] is a suppressor of adult mushroom body | somatic clone phenotype of ssh^1-11

(Ng and Luo, 2004)

Rho1^72O/Rho1[+] is a suppressor of adult mushroom body phenotype of LIMK1^UAS.Tag:HA, Scer\GAL4^ey-OK107

(Ng and Luo, 2004)

Rho1^72O/Rho1[+] is a suppressor of leg | heat sensitive phenotype of Sb^hs.PB

(Bayer et al., 2003)

Rho1^72O is a suppressor of ommatidium phenotype of pk^pk.sev

(Jenny et al., 2003)

Rho1^72O/Rho1[+] is a suppressor of eye phenotype of Rac1^GMR.PN

(Tan et al., 2003)

Rho1^72O/Rho1[+] is a suppressor of wing hair | increased number phenotype of fz^I.hs

(Winter et al., 2001)

NOT Suppressor of

Statement

Reference

Rho1^72O/Rho1[+] is a non-suppressor of wing hair phenotype of Scer\GAL4^en-e16E, kermit^GS2053

(Djiane and Mlodzik, 2010)

Rho1^72O is a non-suppressor of ommatidium phenotype of Scer\GAL4^hs.2sev, pk^sple.UAS

(Jenny et al., 2003)

Rho1^72O is a non-suppressor of ommatidium phenotype of Scer\GAL4^sev.PM181, stan^UAS.cUa

(Das et al., 2002)

Rho1^72O is a non-suppressor of photoreceptor cell R3 | ectopic phenotype of Scer\GAL4^sev.PM181, stan^UAS.cUa

(Das et al., 2002)

Rho1^72O is a non-suppressor of photoreceptor cell R4 phenotype of Scer\GAL4^sev.PM181, stan^UAS.cUa

(Das et al., 2002)

Rho1^72O is a non-suppressor of eye phenotype of Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Rho1^72O is a non-suppressor of eye phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Rho1^72O is a non-suppressor of ommatidium phenotype of Scer\GAL4^hs.2sev, msn^EP549

(Paricio et al., 1999)

Other

Statement

Reference

Rho1^72O, dsh¹ has femur phenotype

(Mieszczanek et al., 2022)

Rho1^72O, dsh^ΔPDZ has femur phenotype

(Mieszczanek et al., 2022)

Rho1^72O, Rok² has myoblast phenotype

(Kim et al., 2015)

GluRIIA^SP16, Rho1^72O/Rho1[+] has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

GluRIIA^SP16, Rho1^72O/Rho1[+], cac^S/cac[+] has embryonic/larval neuromuscular junction phenotype

(Frank et al., 2009)

Rho1^72O/Rho1[+], dia² has embryonic/first instar larval cuticle phenotype

(Homem and Peifer, 2008)

Rho1^72O/Rho1[+], dia² has embryonic head phenotype

(Homem and Peifer, 2008)

Rho1^72O/Rho1[+], dia² has amnioserosa | maternal effect phenotype

(Homem and Peifer, 2008)

Rho1^72O/Rho1[+], Sb^63b has leg phenotype

(Bayer et al., 2003)

Rho1^72O/Rho1[+], Sb⁷⁰ has leg phenotype

(Bayer et al., 2003)

Rho1^72O, Sb^63b has leg phenotype

(Bayer et al., 2003)

Rho1^72O, Sb⁷⁰ has leg phenotype

(Bayer et al., 2003)

Rho1^72O/Rho1[+], zip^Ebr has wing phenotype

(Mizuno et al., 2002)

Rho1^72O, zip^Ebr has wing phenotype

(Mizuno et al., 2002)

Rho1^72O, zip[+]/zip^Ebr has leg phenotype

(Halsell et al., 2000)

Rho1^72O, zip^Ebr has leg phenotype

(Halsell et al., 2000)

Additional Comments

Genetic Interactions

Statement

Reference

Rho1^72O 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 sqh^{E21.T:Zzzz\FLAG} suppresses the myoblast fusion defect seen in Rho1^72O Rok² double mutant embryos.

Expression of sqh^{A20.A21.T:Zzzz\FLAG} does not suppress the myoblast fusion defect seen in Rho1^72O Rok² double mutant embryos.

Rho1^72O enhances the myoblast fusion defects seen in kirre^rP298 mutant embryos.

Expression of sqh^{E21.T:Zzzz\FLAG} partially suppresses the myoblast fusion defects seen in kirre^rP298 Rho1^72O mutant embryos, returning fusion to the level of kirre^rP298 mutants alone.

Rho1^72O enhances the myoblast fusion defects seen in Ced-12⁵⁰ mutant embryos.

Expression of Rho1^{Scer\UAS.P\T.T:Avic\GFP} in founder cells under the control of Scer\GAL4^kirre-rP298 partially suppresses the myoblast fusion defects seen in Ced-12⁵⁰ Rho1^72O mutant embryos, returning fusion to the level of Ced-12⁵⁰ mutants alone. No suppression is seen when Rho1^{Scer\UAS.P\T.T:Avic\GFP} is expressed in fusion-competent myoblasts under the control of Scer\GAL4^sns.PK.

Expression of Fim^{Scer\UAS.T:Avic\GFP-YFP.Venus} significantly rescues the myoblast fusion defects seen in Rho1^72O mutant embryos expressing Rho1^N19.Scer\UAS in founder cells under the control of Scer\GAL4^kirre-rP298.

(Kim et al., 2015)

Maternal heterozygosity for Rho1^72O substantially suppresses the abnormal perpendicular membrane expansion seen at the base of cellularization furrows in embryos derived from females expressing sstn^{dsRNA.shRNA.Scer\UAS.P\T.2} under the simultaneous control of Scer\GAL4^{otu.T:Hsim\VP16}, Scer\GAL4^nos.PG and Scer\GAL4^{nos.UTR.T:Hsim\VP16}.

(Liu et al., 2015)

Maternal heterozygosity for Rho1^72O almost completely suppresses the furrow canal expansion phenotype seen in embryos derived from mothers expressing step^HMS00365 under the control of Scer\GAL4^{mat.αTub67C.T:Hsim\VP16}. The number of endocytic tubules emanating from furrow canals during early cellularisation is restored.

Maternal heterozygosity for Rho1^72O almost completely suppresses the furrow canal expansion phenotype seen in step^SH0323/step^k08110 mutant embryos.

(Lee and Harris, 2013)

An average of 27.8 +/- 5% of Sip1⁰⁶³⁷³/Sip1⁰⁶³⁷³ ; Rho1^72O/+ animals survive to adulthood.

(Hughes et al., 2010)

Rho1^72O dominantly enhances the shortening of the wing which is seen in Drak^KO and in Drak^del flies.

(Neubueser and Hipfner, 2010)

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 Rho1^72O.

The cuticle phenotype of dead embryos derived from baz^G0484/+ embryos derived from a cross of baz^G0484/+ females to wild-type males is enhanced if the females also carry one copy of Rho1^72O.

(Shao et al., 2010)

The Rho1^72O/+ heterozygous mutation can partially suppress the GluRIIA^SP16 NMJ synaptic homeostatic response.

The Exn^EY01953/+ heterozygous mutation does not enhance the Rho1^72O/+, GluRIIA^SP16 double mutant NMJ synaptic homeostasis phenotype.

The combination of Rho1^72O/+ and cac^S/+ heterozygous mutations blocks the synaptic homeostatic compensation at the neuromuscular junction (NMJ) in a homozygous GluRIIA^SP16 genetic background.

(Frank et al., 2009)

Rho1^72O clones expressing dia^{CA.Scer\UAS.T:Ivir\HA1} still exhibit disrupted adherens junctions.

Expression of Rab11^{S25N.Scer\UAS.P\T.T:Avic\GFP-YFP} in Rho1^72O 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.

Cdc42^{dsRNA.Scer\UAS} expression suppresses the adherens junctions defects observed between two Rho1^72O cells but does not suppress the increased apical area.

Expression of Rab5^{S43N.Scer\UAS.P\T.T:Avic\GFP-YFP} in Rho1^72O clones suppresses the adherens junction defect seen between two Rho1^72O cells, although decreased apical tension is not affected.

Expression of Rab5^{Q88L.Scer\UAS.P\T.T:Avic\GFP-YFP} (under the control of Scer\GAL4^Act5C.PI) in Rho1^72O clones does not worsen the Rho1^72O 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 Rho1^72O clones.

Expression of Rab5^GD10492 in Rho1^72O clones suppresses the adherens junction defect seen between two Rho1^72O cells, although decreased apical tension is not affected.

(Warner and Longmore, 2009)

dia² homozygotes in which maternal Rho1 function is reduced (derived from Rho1^72O 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 Rho1^72O 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.

(Homem and Peifer, 2008)

Rho1^72O 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.

(Larson et al., 2008)

The multiple wing hair phenotype caused by expression of tow^Scer\UAS.cCa under the control of Scer\GAL4^hs.PB using heat shock at 24 hours after puparium formation is enhanced if the flies are also carrying one copy of Rho1^72O.

(Chung et al., 2007)

Rho1^72O/+ partially suppresses the wing phenotype of animals expressing rok^cat.Scer\UAS under the control of Scer\GAL4^en-e16E.

(Verdier et al., 2006)

Rho1^72O/+ 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 Csk^IR.Scer\UAS Scer\GAL4^ptc-559.1 third instar larvae.

(Vidal et al., 2006)

Rho1^72O/+ suppresses the mutant wing phenotype caused by expression of LIMK1^Scer\UAS.cCa under the control of Scer\GAL4^en-e16E (the % of wings with normal morphology at 18^oC is increased from 9% to 97%). The frequency of the malformed leg phenotype seen in Sb^63b/+ heterozygotes (8%) is increased if the flies are also heterozygous for Rho1^72O (31%). The frequency of the malformed leg phenotype seen in Sb⁷⁰/+ heterozygotes (7%) is increased if the flies are also heterozygous for Rho1^72O (56%). The frequency of the malformed leg phenotype seen in br¹/Y males (1%) is increased if the flies are also heterozygous for Rho1^72O (12%).

(Chen et al., 2004)

The sti^{dsRNA.Sym.Scer\UAS} Scer\GAL4^ey.PB rough eye phenotype is significantly enhanced by Rho1^72O. The rough eye phenotype associated with the expression of RacGAP50C^{dsRNA.Scer\UAS}, under the regulation of Scer\GAL4^ey.PB in the developing eye imaginal disc is dominantly enhanced by Rho1^72O.

(D'Avino et al., 2004)

Rho1^72O shows a strong interaction (at least 50% of double heterozygotes have at least one malformed leg) with the following mutations: Sb^63b and Sb⁷⁰. The frequency of malformed legs seen in animals in which Sb^hs.PB is expressed in a wild-type background using a 1 hour 37^o heat shock in staged 0 hour or 3 hour prepupae is partially suppressed by Rho1^72O/+.

(Bayer et al., 2003)

The small, rough eye phenotype of Rac1^GMR.PN flies is partially suppressed by heterozygosity for Rho1^72O.

(Tan et al., 2003)

The proportion of symmetrical (R3/R3) ommatidia in the eyes of stan^Scer\UAS.cUa; Scer\GAL4^sev.PM181 flies is unaffected by heterozygosity for Rho1^72O.

(Das et al., 2002)

92% of Rho1^72O/zip^Ebr double heterozygotes have a malformed leg phenotype. 16% of Rho1^72O/Df(2R)Jp1 double heterozygotes show a malformed phenotype.

(Halsell et al., 2000)

Has no effect on the ommatidial polarity phenoptype seen in flies with msn^EP549 driven by Scer\GAL4^hs.2sev.

(Paricio et al., 1999)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Rho1^E3.10

(Halsell et al., 2000)

Rho1^J3.8

(Halsell et al., 2000)

Rescued by

Rho1^72O is rescued by Scer\GAL4^Act5C.PI/Rho1^UAS.cMa

(Warner and Longmore, 2009)

Comments

Rho1^72O clones are rescued by expression of Rho1^Scer\UAS.cMa. In some cases, a decrease in the apical area is observed, perhaps due to the high level of Rho1^Scer\UAS.cMa overexpression.

(Warner and Longmore, 2009)

Rho1^Scer\UAS.cMa rescues the dendrite phenotype of homozygous Rho1^72O mushroom body neuroblast clones when expressed under the control of Scer\GAL4^Tab2-201Y, without altering the proliferation defect.

(Lee et al., 2000)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

7325

y¹ w^*; Rho1^72O/CyO, P{sevRas1.V12}FK1

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (11)

Reported As

Symbol Synonym

DRho1^72O

(Mizuno et al., 2002)

Rho1⁷²⁰

(Hughes et al., 2010, Warner and Longmore, 2009, Sweeney et al., 2008, Verdier et al., 2006, Chen et al., 2004, D'Avino et al., 2004, Tan et al., 2003, Sullivan and Rubin, 2002)

Rho1^72O

(Sarpal et al., 2019, Greer et al., 2013, Lee and Harris, 2013, Matsuda et al., 2013, Frank et al., 2009, Homem and Peifer, 2008, Larson et al., 2008, Polaski et al., 2006, Paladi and Tepass, 2004)

RhoA⁷²⁰

(Thuveson et al., 2019, Echard and O'Farrell, 2003, Paricio et al., 1999)

RhoA^72O

(Mieszczanek et al., 2022, Chung et al., 2007, Wilson et al., 2005, Ng and Luo, 2004, Bayer et al., 2003, Bloor and Kiehart, 2002, Billuart et al., 2001, Bloor and Kiehart, 2001, Winter et al., 2001, Halsell et al., 2000, Lee et al., 2000, Asha et al., 1999)

dRhoA^72O

(Das et al., 2002)

rho1⁷²⁰

(Jacinto et al., 2002)

rho1^72O

(West et al., 2017, Kim et al., 2015, Liu et al., 2015, Neubueser and Hipfner, 2010)

rho^A72o

(Jenny et al., 2003)

rhoA⁷²⁰

(Jenny et al., 2005, Brumby et al., 2004)

rhoA^72O

(Djiane and Mlodzik, 2010, Chung et al., 2009)

Name Synonyms

Secondary FlyBase IDs

References (52)

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