FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\rho6
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General Information
Symbol
Dmel\rho6
Species
D. melanogaster
Name
FlyBase ID
FBal0017860
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
rhodel1
Key Links
Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

5.0kb segment has been deleted that includes the Ecol\lacZ of the P{lacW} and 0.5-0.8kb of flanking genomic sequences at the 5' end of the transposase-Ecol\lacZ fusion.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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
Detailed Description
Statement
Reference

The proliferation of rho6 mutant clones of adult midgut progenitor cells is normal.

Virtually all eggs derived from egg chambers containing complete homozygous follicle cell clones appear normal and have two dorsal appendages.

Only 15% of eggs derived from females with mosaic rho6 egg chambers show defects in dorsal appendage size or inter-appendage distance.

When homozygous somatic clones are made, they proliferate normally, and differentiate bristles but do not differentiate bracts.

The number of limb primordial cells is the same as controls in stage 11 embryos, while the number of leg disc cells is reduced in stage 15 embryos. The number of wing disc cells is increased.

Homozygous mutant clones cause vein-loss phenotypes, sometimes extending a few cells outside the clone boundary. In other cases, vein truncation is rescued within the border of the clone. These reciprocal forms of local cell non-autonomy appear to depend on the shape of the clone, an island of cells tend to take on the vein phenotype associated with the surrounding cells. Homozygous mutant clones on the dorsal side of the wing tended to remove both dorsal and ventral components of the wing vein, however ventral clones generally only affected the ventral components. Homozygous Minute clones revealed that wing veins L1, L2, L3, and L4 are often almost completely eliminated, though for L3, and L4 only the distal halves of the vein are typically affected. The anterior marginal vein L1 is never affected. The overall pattern of vein loss is very similar to SX155 clones, though clones lacking SX155 seem to have slightly stronger vein-loss phenotypes extending more proximally than rho6.

Individual denticle rows are not well defined in mutant embryos. Row 5 denticles can be seen in the middle of the mutant denticle belts. Anterior to row 5 is a row consisting of small, stubby denticles, and the most anterior row of denticles contains sparse row 2 denticles. All of the denticles in rho6 SerRX106 double mutant embryos are similar to each other and resemble a composite of type 5 and 2 denticles. The denticles are disorganised and separate rows are not distinguishable.

Early CNS development shows mild abnormalities in mutant embryos: three neuroblast columns form but there is a weak decrease in the formation of intermediate neuroblasts and their progeny and a weak mis-specification of medial neuroblasts.

sna-positive neuroblasts are often missing in homozygous embryos. Loss of RP2 motor neurons is also seen.

Dorsal medial cell numbers vary between 6 and 10 per embryo.

Homozygous embryos show a loss of 3 chordotonal organs per abdominal hemisegment (VChA and two in LCh5).

rho6/rho7M43 embryos exhibit deletion of the ventral denticles so the width of the belt is reduced. Keilin's organs are missing or defective. Wing, leg, haltere and eye/antenna rho6/rho7M43 mutant discs can be in vivo cultured.

Loss of two of five Ch organs at LCh5 and one ventral Ch organ in all abdominal segments. rho6 argos257 double mutants exhibit the same phenotype as the rho6 single mutant.

Cuticular phenotype similar to rho7M43.

strong allele embryonic lethal

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
NOT suppressed by
Statement
Reference

rho6 has phenotype, non-suppressible by Scer\GAL4Bx-MS1096/SUAS.cGb

NOT Suppressor of
Statement
Reference

rho6 is a non-suppressor of dorsal appendage phenotype of cicfet-U6/cicfet-T6

rho6 is a non-suppressor of egg phenotype of cicfet-U6/cicfet-T6

Additional Comments
Genetic Interactions
Statement
Reference

rho6 mutant clones have no effect on the ectopic appendage-producing fates in cicfet-U6/cicfet-T6 mutant egg chambers, indicating that loss of rho function cannot suppress the cic phenotype.

The disc phenotype of tkv8 ; rho6 double mutant embryos is a simple addition of each single mutant phenotype, in which wing discs are lost completely and leg discs are severely reduced.

Expression of SScer\UAS.cGb directed by Scer\GAL4Bx-MS1096 in homozygous rho6 clones does not suppress the rho6 phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer

Bier.

Comments
Comments

No interaction with P{sev-svp1} or P{sev-svp2} exists.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (24)