A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\RhoGEF204291

General Information
SymbolDmel\RhoGEF204291SpeciesD. melanogaster
NameFlyBase IDFBal0008055
Feature typealleleAssociated geneDmel\RhoGEF2
Also Known AsDRhoGEF2l(2)04291, DrhoGEF204291, l(2)04291
Map ( GBrowse ) Untitled Document detailed view FBti0039757 FBti0009121 FBti0011126 FBti0041748 FBti0077658
Allele classloss of function allele
MutagenP-element activity
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Description
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FB2013_03
FB2013_02
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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
P{PZ} element insertion in an intron that interrupts the 5' UTR.
P{PZ} insertion in the second intron.
Insertion of a P{PZ} element within a 1.3kb intron at the 5' end of the gene.
Caused by insertion
Cytology
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hide Phenotype Manifest In
cortical actin cytoskeleton & syncytial blastoderm embryo | maternal effect
pole cell & cytoskeleton | germ-line clone
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Statement
Reference
Multinucleate cells are present in 100% of RhoGEF2[04291] embryos during cellularisation, and disruptions in the furrow array are observed in these animals.
Embryos in the offspring of homozygous RhoGEF2[04291] mothers display areas of decreased actin as well as areas of excessive actin associated with rings. Actin does not remain in apical caps during metaphase in these embryos. Actin pseudocleavage furrows often appear thickened in cross-sections in mutant embryos, but they do not show extension defects.
The two lateral rows of midline cells fail to form in mutant embryos, due to a failure of mesoderm internalisation.
Embryos that are both maternally and zygotically mutant for RhoGEF204291 show spiracle defects; 34% show a failure of spiracle invagination, 26% have lumen defects and 3.5% show both defects.
Embryos derived from RhoGEF204291 germline clones contain a variable proportion of multinucleate cells.
The following phenotypes are observed in embryos derived from RhoGEF204291 germ-line clones (paternal rescue was not observed): 1) The depth of metaphase furrows at cycle 13 is more variable than wild type; some furrows break down or fail to invaginate which can cause adjacent mitotic spindles to collide and leads to the elimination of nuclei from the cortex. 2) During the slow phase of cellularization, actin rings appear rounded instead of hexagonal and are irregular in size, nuclei are wider than in wild type, and multinucleated actin rings are frequently observed. 3) When the cellularization front reaches the base of the nuclei, actin rings stay in proximity to each other rather than constricting. 4) During the subsequent fast phase of cellularization, actin rings are irregular in size and many multinucleated rings remain very large. During cellularization, embryos derived from RhoGEF204291 germ-line clones do not exhibit a decrease in the rate of membrane invagination but do show irregular radial movement of nuclei, with some nuclei remaining apical. Embryos derived from RhoGEF204291 germ-line clones show a hole in their ventral cuticle. The following defects are observed during pole cell formation in embryos derived from RhoGEF204291 germ-line clones: pole cells form but show an uneven distribution of actin; after nuclear division cycle 10, the pole cells fail to form independent cortical actin structures to separate them from the somatic nuclear layer; during cellularization, nuclei are eliminated from the cortex and accumulate in the yolk at the posterior pole, while the pole cells remain embedded in the somatic nuclear layer rather than sitting on top of the syncytium; finally, the invaginating cellularization front obliterates the majority of the pole cells in the RhoGEF204291 mutants.
Homozygotes die during late embryogenesis or early larval stages with no obvious phenotype. Embryos derived from germline mosaics develop with ventral open cuticles. Deep transverse folds form during germ band elongation. The posterior and anterior midguts fail to invaginate. Apical constriction of cells along the ventral midline at the beginning of gastrulation is severely disrupted. Cell shape changes appear to occur at random and no invagination is formed, phenotype suggests loss of an instructive signal.
Germline clones produce eggs with patterning defects: ventral hypoderm is absent.
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Statement
Reference
RhoGEF204291, zipEbr has visible | dominant phenotype, suppressible by Mbs3
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Statement
Reference
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Statement
Reference
RhoGEF204291/RhoGEF2[+] is a suppressor of visible phenotype of LIMK1Scer\UAS.cCa, Scer\GAL4en-e16E
RhoGEF204291 is a suppressor of lethal | male phenotype of flw6
RhoGEF204291 is a suppressor of visible phenotype of Rho1GMR.PH
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Statement
Reference
Rho1J3.8, RhoGEF204291/RhoGEF2[+] has visible phenotype
RhoGEF204291/RhoGEF2[+], Sb70 has visible | dominant phenotype
RhoGEF204291/RhoGEF2[+], zipEbr has visible phenotype
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Statement
Reference
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Statement
Reference
RhoGEF204291, zipEbr has wing phenotype, suppressible by Mbs3
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Statement
Reference
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Statement
Reference
RhoGEF204291/RhoGEF2[+] is a suppressor | partially of oocyte | somatic clone phenotype of flwFP41
RhoGEF204291/RhoGEF2[+] is a suppressor of wing phenotype of LIMK1Scer\UAS.cCa, Scer\GAL4en-e16E
RhoGEF204291 is a suppressor of eye phenotype of Rho1GMR.PH
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Statement
Reference
RhoGEF204291/RhoGEF2[+], Sb63b has leg phenotype
RhoGEF204291/RhoGEF2[+], Sb70 has leg phenotype
RhoGEF204291/RhoGEF2[+], zipEbr has wing phenotype
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Statement
Reference
One copy of RhoGEF2[04291] partially suppresses the oocyte polarity defects seen when the posterior follicle cells are mutant for flw[FP41].
The progeny of dia[2] RhoGEF2[04291] double heterozygous females have abnormal protrusions extending from amnioserosa cells over the adjacent epidermis during dorsal closure.
Embryos that are both maternally and zygotically mutant for RhoGEF204291 and are also heterozygous or homozygous for Gef64C1 show a mild increase in the frequency of spiracle defects compared to embryos that are both maternally and zygotically mutant for RhoGEF204291 in a Gef64C+ background.
Embryos derived from RhoGEF204291 germ-line clones that are also zygotically homozygous for Df(3R)tll-e resemble RhoGEF204291 single mutants (derived form germ-line clones) during syncytial divisions. However, RhoGEF204291, Df(3R)tll-e double mutants show a progressive deterioration in their actin networks during cellularization: they have breaks in actin rings more frequently than the single mutants; toward the end of the slow phase of cellularization, their actin network is severely fragmented with only isolated actin rings being found (although these isolated rings did not constrict prematurely, as is observed in Df(3R)tll-e embryos); and at later stages of cellularization, the actin network network is completely disrupted.
RhoGEF204291/+ 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 87%).
RhoGEF204291 shows a weak interaction (5-24% of double heterozygotes have at least one malformed leg) with the following mutations: Sb63b and Sb70. br1 fails to show a significant genetic interaction (assayed in terms of a malformed leg phenotype) with RhoGEF204291. Sbsbd-201/Sbsbd-1 shows a weak interaction (5-24% of double mutants have at least one malformed leg) with the following mutations: RhoGEF204291/+.
The fraction of flies showing a malformed leg phenotype in at least one leg, for RhoGEF204291 in double heterozygous combination with one of the following alleles is - SbEbr20: 1%, SbEbr48: 2%, SbEbr228: 4%, SbEbr448: 4%, SbEbr536: 2%, SbEbr623: 0%, Rho1Ebr233: 4%, Rho1Ebr246: 17%, bsEbr292: 0%, E(br)24Ebr24: 2%, E(br)65Ebr65: 4%, E(br)155Ebr155: 6%, E(br)165Ebr165: 7%, E(br)333Ebr333: 9%, E(br)72Ebr72: 1%, E(br)121Ebr121: 49%, E(br)160Ebr160: 2%, E(br)187Ebr187: 2%, E(br)420Ebr420: 3% and E(br)444Ebr444: 36%.
38% of RhoGEF204291/zipEbr double heterozygotes have a malformed leg phenotype.
Suppresses the rough eye phenotype caused by Rho1GMR.PH.
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Statement
Reference
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Fails to complement
Rescued by
Comments
The ventral open cuticle defect seen in embryos derived from RhoGEF204291 germ-line clones is rescued when RhoGEF2RE.Scer\UAS is expressed ubiquitously using Scer\GAL4mat.αTub67C.T:Hsim\VP16.
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Bloomington
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Discoverer
A. Spradling.
hide Comments
Precise excision of the P{PZ} element reverts the lethal phenotype and the genetic interaction with zipEbr.
Excision of the P{PZ} insertion reverts the maternal effect demonstrating the insertion is responsible for the mutant phenotype.
Excision of the P{PZ} element demonstrates that the lethality and suppression of the Rho1GMR.PH phenotype of RhoGEF204291 is caused by the P{PZ} element insertion.
Complements: GstS104227. Complements: Sply05091. Complements: l(2)0625306253. Complements: l(2)0665506655. Complements: l(2)k11502k11502. Complements: l(2)k15914k15914.
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hide Synonyms & Secondary IDs ( 10 )
Reported As
Symbol Synonym
DrhoGEF204291
DRhoGEF204291
DRhoGEF2104291
Gef2l(2)04291
l(2)0429104291
 
RhoGEF2l(2)04291
RhoGEF204291
Name Synonym
Secondary FlyBase IDs
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Sun et al., 2011, Development 138(10): 1991--2001
Regulation of somatic myosin activity by Protein Phosphatase 1{beta} controls Drosophila oocyte polarization. [FBrf0213586]