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General Information
Symbol
Dmel\RhoGEF204291
Species
D. melanogaster
Name
FlyBase ID
FBal0008055
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
DRhoGEF2l(2)04291, RhoGEF2l(2)04291, DrhoGEF204291, l(2)04291
Nature of the Allele
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

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.

Insertion components
P{PZ}RhoGEF204291
Product class / Tool use(s)
Encoded product / tool
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

Multinucleate cells are present in 100% of RhoGEF204291 embryos during cellularisation, and disruptions in the furrow array are observed in these animals.

Embryos in the offspring of homozygous RhoGEF204291 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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference

RhoGEF204291, zipEbr has visible | dominant phenotype, suppressible by Mbs3

Enhancer of
Suppressor of
Statement
Reference

RhoGEF204291/RhoGEF2[+] is a suppressor of visible phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E

RhoGEF204291 is a suppressor of lethal | male phenotype of flw6

RhoGEF204291 is a suppressor of visible phenotype of Rho1GMR.PH

Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference

RhoGEF204291, zipEbr has wing phenotype, suppressible by Mbs3

Enhancer of
Suppressor of
Statement
Reference

RhoGEF204291/RhoGEF2[+] is a suppressor | partially of oocyte | somatic clone phenotype of flwFP41

RhoGEF204291/RhoGEF2[+] is a suppressor of wing phenotype of LIMK1UAS.cCa, Scer\GAL4en-e16E

RhoGEF204291 is a suppressor of eye phenotype of Rho1GMR.PH

Other
Additional Comments
Genetic Interactions
Statement
Reference

One copy of RhoGEF204291 partially suppresses the oocyte polarity defects seen when the posterior follicle cells are mutant for flwFP41.

The progeny of dia2 RhoGEF204291 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.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
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.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

A. Spradling.

Comments
Comments

Excision of the P{PZ} insertion reverts the maternal effect demonstrating the insertion is responsible for the mutant phenotype.

Precise excision of the P{PZ} element reverts the lethal phenotype and the genetic interaction with zipEbr.

Complements: GstS104227. Complements: Sply05091. Complements: l(2)0625306253. Complements: l(2)0665506655. Complements: l(2)k11502k11502. Complements: l(2)k15914k15914.

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.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (10)
References (33)