FB2025_01 , released February 20, 2025
Allele: Dmel\rho7M43
Open Close
General Information
Symbol
Dmel\rho7M43
Species
D. melanogaster
Name
FlyBase ID
FBal0017858
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
rho7M, ve4, rhomboid7M43, rho4
Key Links
Nature of the Allele
Progenitor genotype
Cytology
Description
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

larval sense organ & antennal segment

larval sense organ & maxillary segment

Detailed Description
Statement
Reference

rhoL68/rho7M43 mutant embryos exhibit cardioblast (CB) patterning defects, and a significantly decreased number of cardioblasts, namely of generic cardioblasts, leading to a lower generic CBs:ostial CBs ratio than the typical 4:2 ratio. These embryos also exhibit a significant decrease in the number of odd pericardial cells, although even pericardial cells are unaffected, as compared to controls.

R8 differentiation is defective in rho7M43 homozygotes.

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

Only 4% of eggs derived from females with mosaic rho7M43 egg chambers show defects in dorsal appendage size or inter-appendage distance.

Tracheal invagination is alterated from its beginning at early stage 11 in rho7M43 mutant embryos. Instead of a few cells initiating invagination at a precise point and being subsequently followed by the remaining cells, a broad domain of the tracheal primordium appears to bend in a general way, forming a broad cavity. Cells on the dorsal side do not carry out their rotation movement, and an abnormal finger-like structure observed.

In rho7M43 mutant embryos, neither myosin nor actin accumulates tightly around the invagination edge; instead they form aggregates.

In rho7M43 stage 15 embryos, the genital disc precursor cells are completely missing.

Metameric furrow form and are maintained normally in rho7M43 homozygous embryos.

Mutants exhibit a loss of midbrain. Circumesophageal connectives are frequently broken at Embryonic Stage 16.

Border cells still migrate dorsally when all dorsal follicle cells are mutant for rho7M43 in females containing homozygous clones.

The number of chordotonal organs in the lateral cluster is reduced from 5 to 3 in stage 16 homozygous embryos and there is a complete lack of oenocytes.

Homozygous embryos lack muscle DA1 but not pericardial cells.

Homozygous embryos have a reduced number of cells in both the anterior and posterior Malpighian tubules compared to wild-type embryos. The number of cells in the anterior Malpighian tubules is severely reduced in rho7M43 SIIN double mutant embryos.

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.

Stage 12 embryos display lack of dorsal median cells in 7 out of 10 segments. Stage 14 embryos exhibit loss of mesodermal cells.

Embryos lack denticles and often exhibit fusion between the medial regions of alternating denticle belts. CNS commissures are fused. Scer\GAL4sim.P3.7 mediated rhoScer\UAS.cXa expression in mutant embryos greatly reduces the medial fusion of denticle belts. The CNS phenotype is not rescued.

Malpighian tubule elongation is incomplete in homozygous embryos.

Nondefective in gonad assembly.

Salivary placodes are expanded towards the ventral midline.

Anterior and posterior commissure fuse. Initial development of the axon commissures appears normal but the axon tracts fail to separate at the time of midline glia migration. Midline glial cells die early.

No changes in phenotype of tor13D embryos.

rho7M43 embryos have a narrow ventral nervous system and denticle bands. The medial parts of the denticle bands are fused. The ventral arms of the head skeleton are fused. The anal pads, Keilin's organs, maxillary sense organs and antennal sense organs are reduced.

strong allele embryonic lethal

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

rho7M43 has visible phenotype, enhanceable by ru1

Enhancer of
Statement
Reference

rho7M43 is an enhancer of visible phenotype of ru1

NOT Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

rho7M43/rho[+] is a suppressor of visible phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

vn[+], vn1, rho7M43, rho[+] is a suppressor | partially of visible phenotype of Scer\GAL4en-e16E, tumΔE1E.UAS

Other
Phenotype Manifest In
Enhanced by
Enhancer of
Suppressor of
Statement
Reference

rho7M43/rho[+] is a suppressor of eye phenotype of Scer\GAL4GMR.PS, cazKK107486

rho7M43/rho[+] is a suppressor of ommatidium phenotype of Scer\GAL4GMR.PS, cazKK107486

rho7M43/rho[+] is a suppressor of cone cell phenotype of Scer\GAL4GMR.PS, cazKK107486

rho7M43/rho[+] is a suppressor of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

vn[+], vn1, rho7M43, rho[+] is a suppressor | partially of wing phenotype of Scer\GAL4en-e16E, tumΔE1E.UAS

rho7M43/rho[+] is a suppressor of phenotype of Src42ASu(Raf)1-1

NOT Suppressor of
Statement
Reference
Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

A rho7M43 heterozygous background significantly suppresses the cazKK107486-induced rough eye phenotype and rescues the fusion of cone cells in pupal retinae.

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.

Tracheal invagination initiates in rho7M43 btlLG19 double mutants, but rotation of dorsal cells does not occur, as in rho7M43 single mutants. However, a finger-like structure is never formed, instead, the tracheal cells remain as a cavity.

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.

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 G1 arrest or differentiation.

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.

Weakly enhances the eye phenotype produced by activated arm constructs. (either armS44Y.GMR or armS56F.GMR).

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.

Dominantly suppresses the ability of Src42ASu(phl)1-1 to suppress the lethality of phl1/Y flies.

rho7M43, vnddd-4 double mutant embryos show embryonic CNS neuroblast phenotypes that are indistinguishable from those cause by Egfr mutants. Only two neuroblast columns form, RP2 motorneuron almost never forms, half of the MP2s are missing. The 5-2 and MP2 phenotypes are slightly stronger than for Egfrf2.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

rhoScer\UAS.cGa driven by Scer\GAL4rho.654 rescues the oenocyte defect but not the secondary sensory organ precursor cell defects associated with rho7M43.

rho7M43 is both partially rescued by two copies of rhoRyn : 40% of such embryos hatch as viable larvae, with rescued cuticular phenotype. Rescued larvae do not survive to adulthood.

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

Jurgens.

Associated with: ru1.

Comments
Comments

Less than 10% of wild type number of ventral epidermal cells expressing P{lacZ}BP28 are evident in mutant embryos. oc expression is greatly reduced along the midline.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (16)
References (67)