FB2024_03 , released June 25, 2024
Allele: Dmel\ru1
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General Information
Symbol
Dmel\ru1
Species
D. melanogaster
Name
FlyBase ID
FBal0014832
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Mutagen
Nature of the Allele
Progenitor genotype
Cytology
Description

Nucleotide substitution: C?T.

Amino acid replacement: Q55term.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

C1384679T

Reported nucleotide change:

C?T

Amino acid change:

Q55term | ru-PA

Reported amino acid change:

Q55term

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 cardiac chamber of homozygous ru1 mutant flies is abnormally enlarged. Cardiac chamber wall thickness appear thinner in homozygous ru1 flies compared with controls.

Extra cardiac structures in homozygous ru1 flies appear similar to controls. Cardiac parameters of arrhythmia and heart rate are not significantly different between ru1 homozygotes and control flies in intact adults or in dissected hearts perfused with artificial hemolymph.

ru1 homozygotes have a week rough eye phenotype, but R8 differentiation appears normal.

ru1 mutant clones contain normal number of adult midgut progenitor cell clusters.

In stage 16 ru1 mutant embryos, a significant number of ganglionic branch trachea fail to turn posteriorly and dorsally at the ventral midline and instead cross the midline or remain lingering on it.

In ru1 homozygous flies, 64% of ommatidia show rotation defects.

Heterozygous adults exhibit misrotated ommatidia and minor photoreceptor recruitment defects.

The regular array of facets in the eyes of homozygotes produces a rough eye phenotype. There is variable loss of photoreceptors in these mutant eyes, however few defects if any are seen in the recruitment of photoreceptors. Cone cells are dramatically under-recruited, and some pigment cells are seen to be missing.

may overlap wild type Eyes small and rough, have irregular facets and hairs and have black specks from erupted facets. Expression variable; sometimes overlaps wild type. SEM study by Stumm-Tegethoff and Dick (1974).

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

ru1 has visible phenotype, enhanceable by rho7M43

Suppressed by
Statement
Reference
Enhancer of
Statement
Reference

ru1 is an enhancer of visible phenotype of rho7M43

NOT Enhancer of
Statement
Reference

ru1 is a non-enhancer of abnormal cell polarity phenotype of nmoP1

NOT Suppressor of
Statement
Reference

ru1 is a non-suppressor of abnormal cell polarity phenotype of nmoP1

Other
Phenotype Manifest In
Enhanced by
Suppressed by
Statement
Reference

ru1 has ommatidium phenotype, suppressible by sl2/sl2

NOT suppressed by
Statement
Reference
Enhancer of
NOT Enhancer of
Statement
Reference

ru1 is a non-enhancer of ommatidium phenotype of nmoP1

Suppressor of
Statement
Reference

ru[+]/ru1 is a suppressor of eye phenotype of Scer\GAL4GMR.PS, cazKK107486

ru[+]/ru1 is a suppressor of ommatidium phenotype of Scer\GAL4GMR.PS, cazKK107486

ru[+]/ru1 is a suppressor of cone cell phenotype of Scer\GAL4GMR.PS, cazKK107486

NOT Suppressor of
Statement
Reference

ru1 is a non-suppressor of ommatidium phenotype of nmoP1

Other
Additional Comments
Genetic Interactions
Statement
Reference

The net1 phenotype (ectopic veins, vein networking) can be enhanced by combination with CycGHR7 but also by combination with mutant alleles of unrelated factors ru1 or sp1 demonstrating high susceptibility of the net1 phenotype to perturbed genetic background.

A ru1 background suppresses the rough eye phenotype induced by expression of cazKK107486.

A ru1 rho7M43 double mutant background fails to suppress the R1-R7 photoreceptor differentiation defects seen in raspT802 mutant eye disc clones.

ru1/+, rho7M43/+ mutants have normal cardiac function.

Cardiac-specific expression of spis.Scer\UAS driven by Scer\GAL4tin.CΔ4 restores normal cardiac function in homozygous ru1 mutants.

Cardiac-specific expression of spiScer\UAS.cSa driven by Scer\GAL4tin.CΔ4 fails to restore normal cardiac function in homozygous ru1 mutants.

Eyes homozygous for both ru1 and rho7M43 are massively reduced and lack ommatidia.

ru1 rho7M43 Minute clones in the eye disc fail to form the arcs and rosettes of cells in the morphogenetic furrow that are seen in wild-type eye discs. Small clusters of cells can very occasionally be observed in the furrow but these appear at much lower levels than in wild type.

The extra photoreceptor cell phenotype of argosΔ7 clones is enhanced in argosΔ7 Gug14967 clones, with a greater percentage of ommatidia showing supernumerary photoreceptor cells. In contrast, ru1 rho7M43 Gug14967 argosΔ7 mutant clones lack photoreceptor cells.

ru1, rho7M43 embryos show an increased level of apoptosis.

In rho7M43; ru1 double mutant clones in the eye disc, only R8 photoreceptor cells differentiate In rho7M43; ru1; sensE2 triple mutant clones, no photoreceptors differentiate except for a few photoreceptors near the clonal boundary, presumably rescued non-autonomously by neighboring wild-type cell. No rescue of photoreceptor development is seen when these triple mutant clones are made in a rox63 homozygous background.

The defects in ommatidial rotation seen in ru1 homozygotes are almost completely suppressed by sl2/sl2.

69% of cuticles from rho7M43; ru1 double homozygous embryos have at least one denticle belt fusion, compared with 30% in rhounspecified homozygotes. Other aspects of the cuticle phenotype in these double mutants are no stronger than those in rhounspecified embryos. (Note, while the authors do not name an rho allele for this analysis, they do claim to have used a null allele.) Denticle belt fusions in the cuticles of rho7M43; ru1 double homozygous embryos are suppressed by Egfr::tort4021E.hs.sev or Ras85DV12.Scer\UAS with Scer\GAL4prd.RG1, and enhanced by EgfrDN.Scer\UAS (P{UAS-Egfr.DN}29-77-1), Ras85DN17.Scer\UAS or phlK497M.Scer\UAS with Scer\GAL4prd.RG1. The penetrance of denticle belt fusions in the cuticles of rho7M43; ru1 double homozygous embryos is reduced from just under 60% to less than 20% by Df(3L)H99/Df(3L)H99.

In rho7M43; ru1 double mutant somatic clones in the 3rd instar eye disc, photoreceptors R2-R5 fail to undergo or differentiation. Within rho7M43; ru1 double mutant somatic clones there is a failure of G1 arrest in the furrow: all cells except R8s re-enter the cell cycle. Most of these cells fail to progress past G2: most remain in G2 arrest posterior to column 3, but both cells in early mitosis and postmitotic cells can be seen near boundaries with wild-type cells.

Large ru1 rho7M43 vnL6 triple mutant clones in the leg can result in truncations of the tarsus region (for example only three tarsal segments may be present). Mosaic legs which have wild-type tissue at the distal tip show rescue of tarsal development.

Clones of doubly mutant for rho7M43 and ru1 do not survive into adult eyes. When mosaic ommatidia are studied, no mutant R8 photoreceptor cells are seen, while mutant photoreceptor cells R1-7 are seen in between a third and a half of mosaic ommatidia. When imaginal discs are examined, an absence of non-R8 photoreceptor cells are seen, and also a complete loss of cone cells. In these clones an increased level of apoptosis is also seen. Apoptotic cells are seen in two main zones, one just ahead of the advancing morphogenetic furrow, and one towards the posterior of the clone.

ru1/Df(3L)ru-K1 flies have slightly diminished eyes and the facets are rough.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of ruScer\UAS.cYa driven by Scer\GAL4tin.CΔ4 rescues the abnormal enlarged cardiac phenotype of ru1 homozygotes.

Images (1)
Stocks (235)
Notes on Origin
Discoverer

Sturtevant, 14th Feb. 1919.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (26)