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General Information
Symbol
Dmel\Rok2
Species
D. melanogaster
Name
FlyBase ID
FBal0122918
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
drok2
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:

G16632914A

Reported nucleotide change:

G?A

Comment:

G to A nucleotide change at the splice acceptor of the first intron in the coding region. The resulting transcript has a single base deletion of a G at the beginning of exon 2 and encodes only the first 21 amino acids of rok followed by a 35 amino acid random peptide and a stop codon.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

G to A mutation in the conserved splice acceptor site at the 3' end of intron 1. The resulting transcript has a single base deletion of a G at the beginning of exon 2 and encodes only the first 21 amino acids of Rok followed by a 35 amino acid random peptide and a stop codon.

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

filamentous actin & nurse cell | germ-line clone

filamentous actin & oocyte | germ-line clone

mushroom body & axon | somatic clone

plasma membrane & oocyte | germ-line clone

Detailed Description
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.

rok2/Y embryos do not exhibit significant gastrulation defects, compared to controls.

Heterozygosity for rok2 does not results in any defects in leg morphogenesis.

The position of the contractile ring at the end of constriction is unbiased along the apical-basal axis in mutant clones in the follicle cells, in contrast to wild type. The midbody ring is always positioned to the apical side when the mutant cells regain their shape at the end of cell division, as occurs in wild type.

Homozygous clones result in defects in ommatidial rotation and in tissue morphology.

rok2 hemizygous embryos show laterality defects in the proventriculus and anterior midgut. The laterality of the other parts of the embryonic gut, including the hindgut and the posterior part of the midgut is normal in these mutants. The proventriculus and the anterior midgut do not rotate (as in wild-type) in these mutants at stages 15 to 17.

baz and arm planar polarity is strongly defective in rok2 mutants.

Overall length of the tracheal dorsal trunk is normal in mutant stage 16 embryos.

Single cell clones of rok2 exhibit an increased apical cell area. Adherens junctions in multiple cell clones are intact.

Salivary glands fail to invaginate or do not invaginate completely in 9% of homozygous embryos. Invagination often begins with anterior gland cells in the mutant embryos, instead of with dorsal-posterior cells as in wild type. 35% of mutant embryos show salivary gland migration defects, where the distal tip cells turn but the proximal half of the gland does not, and the gland fails to migrate posteriorly.

Homozygous clones in the wing result in a multiple wing hair phenotype.

Homozygous cells in the morphogenetic furrow (in clones that encompass the morphogenetic furrow) show a statistically significant impairment in apical constriction and apicobasal contraction.

rok2 mutant follicle cell clones divide normally, form a monolayered follicular epithelium, and retain polarity. However, these cells fail to adopt a normal shape. As a consequence, the epithelium is flatter in these regions than it is in regions with rok activity. rok2 mutant cells are also stretched compared to neighboring wild-type cells. Furthermore, egg chambers with large follicle cell clones develop abnormal shapes as the cyst bulges outwards in the area of the clones.

Females carrying rok2 germline clones (GLCs) are sterile and lay a relatively small number of eggs, all of which are abnormally shaped. 100% of these eggs exhibit fused flat dorsal appendages and invariably fail to hatch. The eggs are abnormally small in 50% of cases and appear "deflated" in the remaining cases. Further analysis of these GLCs shows that several aspects of oogenesis are defective.

From stage 8 of oogenesis onwards, yolk granules in rok2 GLC oocytes aberrantly accumulate and remain at the oocyte cortex, instead of moving throughout the ooplasm. At stage 11, nurse cell cytoplasmic "dumping" is defective in 97% of egg chamber GLCs with nurse cells largely retaining their cytoplasm. rok2 egg chambers contain between one and four abnormally shaped canals, but no major difference in the overall number of ring canals.

Normal oocyte polarity is not established in rok2 GLC oocytes, although microtubules appear to be well organized.

The actin cytoskeleton is disrupted in rok2 GLC oocytes; subcortical F-actin is disorganized in most oocytes and is characterized by the presence of actin clumps within the oocyte and along the length of the oocyte cortex. Cortical F-actin exhibits a somewhat diffuse organization along the oocyte membrane. Additionally, the F-actin network is perturbed in nurse cells in 86% of rok2 GLCs. Nurse cells lack functional F-actin filaments and contain nuclei of increased size that are not properly localized near the center of the cell.

Oocytes exhibit an altered plasma membrane in 82% of rok2 GLCs. There are frequent deformations along localized regions of the cortical membrane, resulting in protrusions into the oocyte cytoplasm. A significant detachment of the oocyte membrane from the apical membrane of follicle cells can also be observed.

Homozygous axons in clones in the mushroom body extend significantly further than heterozygous neurons in the same mushroom body.

Mutants die before developing into wandering third instar larvae. Homozygous clones in the eye are of a similar size to their wild-type siblings. About 50% of ommatidia show an increase or decrease in photoreceptor numbers. Of those ommatidia with the correct number of photoreceptor cells, 60% are misrotated. Very few ommatidia show aberrant chirality. In homozygous clones in the wing, more than 70% of cells produce multiple wing hairs. Most hairs within the clone maintain a largely distal orientation. The majority of cells in wing clones generate more than one F-actin bundle during prehair initiation. The F-actin based prehairs always initiate at the cell periphery and in the majority of cases maintain a roughly distal orientation. These wing phenotypes are cell autonomous.

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

Drakdel/DrakKO, rok[+]/Rok2 has lethal phenotype, suppressible by flwG0172/flwG0172

Drakdel/DrakKO, rok[+]/Rok2 has lethal phenotype, suppressible by sqhE20.E21

Rok2, zipEbr has visible | dominant phenotype, suppressible by Mbs3

NOT suppressed by
Statement
Reference

Drakdel/DrakKO, rok[+]/Rok2 has lethal phenotype, non-suppressible by sqhA20.A21.Tag:FLAG

Rok2 has lethal | recessive | larval stage phenotype, non-suppressible by sqhA21.Tag:FLAG

Enhancer of
Statement
Reference

rok[+]/Rok2 is an enhancer of visible phenotype of Scer\GAL4hs.PB, towUAS.cCa

Rok2 is an enhancer of visible | recessive phenotype of dsh1

NOT Enhancer of
Statement
Reference

rok[+]/Rok2 is a non-enhancer of visible phenotype of Scer\GAL4en-e16E, kermitGS2053

rok[+]/Rok2 is a non-enhancer of visible | recessive phenotype of Rab2351

Suppressor of
Statement
Reference

Rok2 is a suppressor of lethal | recessive | larval stage phenotype of MoeG0323

rok[+]/Rok2 is a suppressor of visible | heat sensitive phenotype of fzI.hs

NOT Suppressor of
Statement
Reference
Other
Statement
Reference

Rho112-6/Rho1[+], Rok2 has visible phenotype

Sb63b/Sb[+], Rok2 has visible phenotype

Sb[+]/Sb70, Rok2 has visible phenotype

rok[+]/Rok2, zipEbr has visible phenotype

Sb63b, rok[+]/Rok2 has visible | dominant phenotype

Rho1E3.10, rok[+]/Rok2 has visible phenotype

Rho1J3.8, rok[+]/Rok2 has visible phenotype

Sb70, rok[+]/Rok2 has visible | dominant phenotype

Rho1J3.8/Rho1[+], Rok2 has visible | dominant phenotype

Rok2, zip[+]/zipEbr has visible | dominant phenotype

Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference

Rho172O, Rok2 has myoblast phenotype, suppressible by sqhE21.Tag:FLAG

Rok2, zipEbr has wing phenotype, suppressible by Mbs3

Rok2 has wing hair | supernumerary phenotype, suppressible by sqhE20.E21

NOT suppressed by
Statement
Reference

Rho172O, Rok2 has myoblast phenotype, non-suppressible by sqhA20.A21.Tag:FLAG

Enhancer of
Statement
Reference

rok[+]/Rok2 is an enhancer of wing hair | supernumerary phenotype of Scer\GAL4hs.PB, towUAS.cCa

Rok2 is an enhancer of wing hair | supernumerary phenotype of dsh1

NOT Enhancer of
Statement
Reference

rok[+]/Rok2 is a non-enhancer of ommatidium phenotype of Scer\GAL4hs.2sev, nmoUAS.cUa

rok[+]/Rok2 is a non-enhancer of wing hair phenotype of Scer\GAL4en-e16E, kermitGS2053

rok[+]/Rok2 is a non-enhancer of wing hair phenotype of Rab2351

rok[+]/Rok2 is a non-enhancer of wing hair | supernumerary phenotype of Scer\GAL4en-e16E, pbldsRNA.UAS

Suppressor of
Statement
Reference

Rok2 is a suppressor of wing | pupal stage | heat sensitive phenotype of PtenJF01859, Scer\GAL4en.PU, Scer\GAL80ts.αTub84B

rok[+]/Rok2 is a suppressor | partially of eye phenotype of Scer\GAL4arm.PS, aurAIM, aurAUAS.cWa

rok[+]/Rok2 is a suppressor | partially of eye phenotype of Rac1GMR.PN

rok[+]/Rok2 is a suppressor of wing hair | supernumerary phenotype of fzI.hs

NOT Suppressor of
Other
Additional Comments
Genetic Interactions
Statement
Reference

Rok2/Rok2 or Rok2 hemizygosity fails to suppress the embryonic lethality and dorsal closure defects seen in embryos expressing crbY10A in a crbGX24w-/crb11A22 background.

Rho172O Rok2 double zygotic mutants exhibit myoblast fusion defects.

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.

Heterozygosity significantly enhances the multiple hair cell phenotype of Scer\GAL4en.PU cmbScer\UAS.RA wings.

rok2 clones generated in PtenJF01859-expressing tissue suppresses the effect of the expression of PtenJF01859 under the control of Scer\GAL80ts.αTub84B and Scer\GAL4en.PU on cell packing, namely the excess of short junctions. Despite a slightly higher proportion of non-rearranging junctions (1.15-fold), the rearranging junctions neither produce an excess of short junctions nor fluctuate extensively, but lengthen to produce long cell junctions as observed in wild-type tissue. Furthermore, the packing and cell rearrangement dynamics in the double mutant tissue is similar to the one observed in rok2 single mutant tissue.

A rok2/+ heterozygous background suppresses the enhanced lethality of aurWK females bearing one copy of sqhE20.E21, and ameliorates the enhanced rough eye phenotype of these flies.

A rok2/+ heterozygous background suppresses the enhanced lethality of aurIM females bearing one copy of sqhE20.E21, and ameliorates the enhanced rough eye phenotype of these flies.

More than half of Drakdel rok2/Drakdel third instar larvae are missing random elements of the tracheal tree.

The wing discs of Drakdel rok2/DrakKO third instar larvae are composed of unusually thin epithelial layers which are grossly distorted. The wing pouch region has folds which project basally out of the plane of the epithelium, and these distortions are accompanied by massive apoptosis.

100% of Drakdel rok2 double homozygous embryos die before hatching. They show a fully penetrant head defect, which is characterized by an anterior hole in the embryonic cuticle and anterior malformations of the cephalopharyngeal skeleton.

rok2 does not exhibit dominant genetic interaction with Rab2351.

Expression of diaGD9442 in rok2 MARCM clones does not affect mature epithelial adherens junctions. An increase in apical area is found, compared to rok2 clones.

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 rok2.

A rok2/+ background does not affect the Scer\GAL4hs.2sev>shgdCR3h.Scer\UAS.T:Avic\GFP-rs ommatidial phenotype.

Neither the reduction in compartment size nor the percentage of cells with multiple wing hairs in pbldsRNA.Scer\UAS; Scer\GAL4en-e16E flies is enhanced by rok2/+.

rok2 shows a strong interaction (at least 50% of double heterozygotes have at least one malformed leg) with the following mutations: Sb70. rok2 shows a moderate interaction (25-49% of double heterozygotes have at least one malformed leg) with the following mutations: Sb63b. rok2 shows a weak interaction (5-24% of double heterozygotes have at least one malformed leg) with the following mutations: Df(3R)sbd105 and Rho112-6. Sbsbd-201/Sbsbd-1 shows a weak interaction (5-24% of double mutants have at least one malformed leg) with the following mutations: rok2/+.

The small, rough eye phenotype of Rac1GMR.PN flies is partially suppressed by heterozygosity for rok2.

Addition of rok2 to dsh1 mutants results in a 2.5-fold increase in the number of multiple wing hair cells compared to dsh1 single mutants. 4% of rok2/Y ; sqhE20.E21/+ flies survive to adulthood. The multiple wing hair phenotype caused by rok2 is almost completely suppressed by sqhE20.E21.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (40)