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General Information
Symbol
Dmel\rho
Species
D. melanogaster
Name
rhomboid
Annotation Symbol
CG1004
Feature Type
FlyBase ID
FBgn0004635
Gene Model Status
Stock Availability
Gene Snapshot
rhomboid (rho) encodes an intra-membrane serine protease that processes the membrane precursors of Egfr ligands. Its roles include growth regulation, cell survival and developmental patterning. [Date last reviewed: 2019-03-14]
Also Known As
ve, Rho1, rhomboid-1, rho-1, veinlet
Key Links
Genomic Location
Cytogenetic map
Sequence location
3L:1,463,811..1,468,944 [+]
Recombination map
3-0.5
Sequence
Other Genome Views
The following external sites may use different assemblies or annotations than FlyBase.
Function
GO Summary Ribbons
Gene Group (FlyBase)
Protein Family (UniProt)
Belongs to the peptidase S54 family. (P20350)
Molecular Function (GO)
[Detailed GO annotations]
Experimental Evidence
Predictions / Assertions
Summaries
Pathway (FlyBase)
Epidermal Growth Factor Receptor Ligand Production -
Factors required for the proteolytic cleavage and/or secretion of transforming growth factor-α-like Egfr ligands spi, Krn or grk.
Gene Group (FlyBase)
RHOMBOID PROTEASES -
Rhomboid proteases are intramembrane serine proteases related to rho, that cleave other transmembrane proteins within their transmembrane domains. Rhomboid proteases are best characterized for their role in epidermal growth factor signaling, where they are required for the production the soluble, secreted ligand. (Adapted from FBrf0235672).
Protein Function (UniProtKB)
Acts early in embryonic development to establish position along the dorsoventral axis and then again later to specify the fate of neuronal precursor cells. Involved in EGF receptor signaling; cleaves Spitz to release the active growth factor.
(UniProt, P20350)
Phenotypic Description (Red Book; Lindsley and Zimm 1992)
ve: veinlet (E. Bier)
thumb
ve: veinlet
From Duncan, 1935, Am. Naturalist 69: 94-96.
Viable alleles exhibit wing venation defects; strong alleles are embryonic lethal. In flies homozygous for viable alleles the L3, L4, and L5 veins do not reach the wing margins (Duncan; Waddington). Developmentally, veins appear complete in prepupa but distal tips are obliterated during the contraction period (Waddington, 1939, 1940). The shortened-vein phenotype is suppressed by px (Waddington), net, and su(ve), and is enhanced by vn, H, Ax, ci, tg2, and ri (Waddington; Diaz-Benjumea and Garcia-Bellido, 1990, Wilhelm Roux's Arch. Dev. Biol 198: 336-54.). Vein-specific modifiers, such as gp, (Bridges and Morgan, 1919, Carnegie Inst. Washington Publ. No. 278: 208) or PL(2)L4a (Thompson, 1976), interact with the effect of ve on L4. The L5 vein seldom extends beyond the posterior crossvein. ve2 is a stronger allele, in which the L2 is also affected (Bertschmann); L2 vein occasionally complete (Thompson, 1976), but other veins do not overlap wild type. Distribution of sense organs (campaniform sensilla and bristles) on L3 is shifted proximally in ve (Spivey and Thompson) When a ve stock is selected for shortened veins, the F1 produced by mating wild-type males to mutant females show terminal gaps in L5 (Thompson and Thoday, 1976). ve/ve/+ intersexes are veinlet, whereas ve/ve/+ triploids are normal, according to Pipkin. Interestingly flies heterozygous for ve and strong embryonic lethal alleles display less severe veinlet phenotypes than ve homozygotes (Bier et al.; Diaz-Benjumea and Garcia-Bellido); furthermore, ve1/ve5 flies appear wild type (Bier, unpublished). Homozygous ve5 embryos exhibit three major types of defects: (1) Dorsoventral defects: Embryos exhibit a deletion of epithelial cells derived from a ventrolateral strip of the blastoderm fate map (i.e., loss of mediolateral cuticular denticles and sensory structures). Other phenotypes resulting from blastoderm patterning defects include failure to complete dorsal closure and development of an abnormal pointed head skeleton (Jurgens et al.; Mayer and Nusslein-Volhard). (2) Midline defects: Mesectodermal cells giving rise to glia and unpaired neurons are abnormal or fail to form. Late developmental consequences include a narrower CNS and pathfinding abnormalities (Mayer and Nusslein-Volhard). (3) Peripheral-nervous-system defects: Two stretch receptor organs (lateral abdominal chordotonal organs) fail to form in lethal ve mutants. The primary chordotonal-organ-precursor cells are likely to be affected since the four progeny sensory-organ cells derived from that precursor cell are missing as a group (Bier et al.). Other late embryonic defects include loss of longitudinal body-wall muscles, ventrally displaced muscle-attachment sites (Bier et al.), and loss of the first row of denticles in abdominal segments (Mayer and Nusslein-Volhard).
Summary (Interactive Fly)
serine protease - transmembrane protein involved with Epidermal growth factor receptor signaling - required for the production or processing of Spitz, the Egfr ligand
Gene Model and Products
Number of Transcripts
2
Number of Unique Polypeptides
1

Please see the GBrowse view of Dmel\rho or the JBrowse view of Dmel\rho for information on other features

To submit a correction to a gene model please use the Contact FlyBase form

Protein Domains (via Pfam)
Isoform displayed:
Pfam protein domains
InterPro name
classification
start
end
Protein Domains (via SMART)
Isoform displayed:
SMART protein domains
InterPro name
classification
start
end
Comments on Gene Model
Tissue-specific extension of 3' UTRs observed during later stages (FBrf0218523, FBrf0219848); all variants may not be annotated
Gene model reviewed during 5.42
Gene model reviewed during 5.46
Gene model reviewed during 5.52
Sequence Ontology: Class of Gene
Transcript Data
Annotated Transcripts
Name
FlyBase ID
RefSeq ID
Length (nt)
Assoc. CDS (aa)
FBtr0072694
2531
355
FBtr0333207
3000
355
Additional Transcript Data and Comments
Reported size (kB)
2.9, 2.5 (northern blot)
Comments
External Data
Crossreferences
Polypeptide Data
Annotated Polypeptides
Name
FlyBase ID
Predicted MW (kDa)
Length (aa)
Theoretical pI
RefSeq ID
GenBank
FBpp0072578
39.3
355
5.12
FBpp0305409
39.3
355
5.12
Polypeptides with Identical Sequences

The group(s) of polypeptides indicated below share identical sequence to each other.

355 aa isoforms: rho-PA, rho-PB
Additional Polypeptide Data and Comments
Reported size (kDa)
355 (aa); 39 (kD)
Comments
External Data
Crossreferences
InterPro - A database of protein families, domains and functional sites
Linkouts
Sequences Consistent with the Gene Model
Mapped Features

Click to get a list of regulatory features (enhancers, TFBS, etc.) and gene disruptions (point mutations, indels, etc.) within or overlapping Dmel\rho using the Feature Mapper tool.

External Data
Crossreferences
Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
Linkouts
Gene Ontology (36 terms)
Molecular Function (1 term)
Terms Based on Experimental Evidence (1 term)
CV Term
Evidence
References
Terms Based on Predictions or Assertions (1 term)
CV Term
Evidence
References
inferred from biological aspect of ancestor with PANTHER:PTN000533014
(assigned by GO_Central )
inferred from sequence model
Biological Process (29 terms)
Terms Based on Experimental Evidence (29 terms)
CV Term
Evidence
References
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
inferred from mutant phenotype
(assigned by UniProt )
inferred from mutant phenotype
inferred from mutant phenotype
(assigned by UniProt )
inferred from mutant phenotype
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:abd-A; FB:FBgn0000014
inferred from mutant phenotype
inferred from genetic interaction with FLYBASE:abd-A; FB:FBgn0000014
inferred from mutant phenotype
(assigned by UniProt )
inferred from mutant phenotype
(assigned by UniProt )
inferred from direct assay
inferred from mutant phenotype
(assigned by UniProt )
inferred from mutant phenotype
inferred from mutant phenotype
Terms Based on Predictions or Assertions (0 terms)
Cellular Component (6 terms)
Terms Based on Experimental Evidence (5 terms)
CV Term
Evidence
References
inferred from direct assay
inferred from high throughput direct assay
inferred from direct assay
inferred from direct assay
Terms Based on Predictions or Assertions (1 term)
CV Term
Evidence
References
Expression Data
Expression Summary Ribbons
Colored tiles in ribbon indicate that expression data has been curated by FlyBase for that anatomical location. Colorless tiles indicate that there is no curated data for that location.
For complete stage-specific expression data, view the modENCODE Development RNA-Seq section under High-Throughput Expression below.
Transcript Expression
in situ
Stage
Tissue/Position (including subcellular localization)
Reference
dorsal ectoderm anlage

Comment: anlage in statu nascendi

ectoderm anlage

Comment: anlage in statu nascendi

mesectoderm anlage

Comment: anlage in statu nascendi

ventral ectoderm anlage

Comment: anlage in statu nascendi

antennal anlage in statu nascendi

Comment: reported as procephalic ectoderm anlage in statu nascendi

dorsal head epidermis anlage in statu nascendi

Comment: reported as procephalic ectoderm anlage in statu nascendi

visual anlage in statu nascendi

Comment: reported as procephalic ectoderm anlage in statu nascendi

organism | restricted | ventro-lateral

Comment: ventro-lateral stripe

organism | ventro-lateral

Comment: in a stripe 7-8 cells wide

northern blot
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data
In the wing pouch, rho is expressed in presumptive wing veins L3, L4, and L5, and in two stripes parallel to the D/V compartment boundary. Expression is also observed in the presumptive wing hinge and mesonotum regions. No transcript is observed in the haltere disc. rho transcript is expressed in the presumptive hinge region of the haltere disc, but not in the haltere pouch.
rho transcript is expressed in concentric ring pattern in leg discs.
Expression pattern inferred from unspecified enhancer trap line.
As the Malphighian tubules start to evert, rho transcript is detected in the tip mother cell, and subsequently in the tip cell.
rho is expressed in follicle cells and in the germline during oogenesis. At oogenesis stage S9, it is expressed in a broad group of cells in the dorsal-anterior end of the egg chamber and by stage S10, expression is restricted to two dorsal-anterior stripes corresponding to the sites of future dorsal respiratory appendages. The early and late oogenesis expression patterns are expanded in fs(1)K10 mutants. In grk and FBgn0003731:Egfr mutants, the early oogenisis pattern is unaffected but the late pattern shows severe restriction of cells expressing FBgn0004635:rho @.
rho is expressed in wandering third instar larvae and in early prepupae in a pattern of intersecting stripes that is likely to be the wing vein primordia. Later, its expression is restricted to developing veins.
rho transcripts are detected in embryos, pupae, and adults on northern blots.
rho is expressed in a complex pattern during embryogenesis. Expression is first observed at the cellular blastoderm stage in two ventrolateral domains, 7-8 cells wide separated by a 13-15 cell wide unlabeled ventral strip. These domains become narrower and modulated in intensity along the A/P axis. As the mesoderm invaginates, the label moves ventrally and becomes restricted to a single row of cells on either side of the midline. Expression continues in these cells as they meet to form the mesectoderm and persists until germ band retraction. During germ band extension, strong expression is seen in cells that will form tracheal pits and in a single large cell dorsal and posterior to the tracheal pit that is thought to be the precursor of chordotonal organs. During germ band retraction, expression begins in the CNS in a segmentally repeated pattern. At the end of germ band retraction, cells forming the anterior-most row in each abdominal segment are labelled both dorsally and ventrally. In the thoracic segments, only the dorsal cells are labelled.
Marker for
 
Subcellular Localization
CV Term
Polypeptide Expression
No Assay Recorded
Stage
Tissue/Position (including subcellular localization)
Reference
immunolocalization
Stage
Tissue/Position (including subcellular localization)
Reference
Additional Descriptive Data
ve protein is localized predominantly on the apical surface of the dorsal anterior follicle cells.
ve protein is expressed in the germline and in dorsal anterior follicle cells during oogenesis. In early stages of oogenesis, it is expressed in a broad group of cells in the dorsal-anterior end of the egg chamber and in later stages, expression is restricted to two dorsal-anterior stripes
ve protein is expressed in the third instar larval eye disc posterior to the morphogenetic furrow. Staining is restricted to the ommatidia and occurs mainly in receptor cells R2, R5, and R8.
Marker for
 
Subcellular Localization
CV Term
Evidence
References
inferred from direct assay
inferred from high throughput direct assay
inferred from direct assay
inferred from direct assay
Expression Deduced from Reporters
Reporter: P{A92}rhoAA69
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{GAL4-ve.L}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lacW}rho5
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lacZ}rho-R1.1
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{lwB}X81
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{Rho(ve)-lacZ.EE}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{rho-lacZ.654}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{rho-lacZ.BAD}
Stage
Tissue/Position (including subcellular localization)
Reference
Reporter: P{veNEE-lacZ}
Stage
Tissue/Position (including subcellular localization)
Reference
High-Throughput Expression Data
Associated Tools

GBrowse - Visual display of RNA-Seq signals

View Dmel\rho in GBrowse 2
RNA-Seq by Region - Search RNA-Seq expression levels by exon or genomic region
Reference
See Gelbart and Emmert, 2013 for analysis details and data files for all genes.
Developmental Proteome: Life Cycle
Developmental Proteome: Embryogenesis
External Data and Images
Linkouts
BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
FLIGHT - Cell culture data for RNAi and other high-throughput technologies
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
Images
Alleles, Insertions, and Transgenic Constructs
Classical and Insertion Alleles ( 32 )
For All Classical and Insertion Alleles Show
 
Other relevant insertions
Transgenic Constructs ( 39 )
For All Alleles Carried on Transgenic Constructs Show
Transgenic constructs containing/affecting coding region of rho
Transgenic constructs containing regulatory region of rho
Deletions and Duplications ( 9 )
Phenotypes
For more details about a specific phenotype click on the relevant allele symbol.
Lethality
Allele
Other Phenotypes
Allele
Phenotype manifest in
Allele
chordotonal organ | precursor & embryonic abdomen
chordotonal organ precursor cell & ventral thoracic disc, with Scer\GAL4sca-109-68
embryonic head & external sensory organ
embryonic thorax & external sensory organ
embryonic trachea & cortical actin cytoskeleton
larval sense organ & antennal segment
larval sense organ & maxillary segment
Orthologs
Human Orthologs (via DIOPT v7.1)
Homo sapiens (Human) (3)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
8 of 15
Yes
No
7 of 15
No
No
5 of 15
No
No
Model Organism Orthologs (via DIOPT v7.1)
Mus musculus (laboratory mouse) (3)
Species\Gene Symbol
Score
Best Score
Best Reverse Score
Alignment
Complementation?
Transgene?
7 of 15
Yes
No
7 of 15
Yes
No
4 of 15
No
No
Rattus norvegicus (Norway rat) (3)
7 of 13
Yes
No
6 of 13
No
No
4 of 13
No
No
Xenopus tropicalis (Western clawed frog) (1)
2 of 12
Yes
No
Danio rerio (Zebrafish) (3)
6 of 15
Yes
No
6 of 15
Yes
No
4 of 15
No
No
Caenorhabditis elegans (Nematode, roundworm) (2)
8 of 15
Yes
No
5 of 15
No
No
Arabidopsis thaliana (thale-cress) (3)
1 of 9
Yes
Yes
1 of 9
Yes
Yes
1 of 9
Yes
No
Saccharomyces cerevisiae (Brewer's yeast) (0)
No records found.
Schizosaccharomyces pombe (Fission yeast) (0)
No records found.
Orthologs in Drosophila Species (via OrthoDB v9.1) ( EOG09190BLJ )
Organism
Common Name
Gene
AAA Syntenic Ortholog
Multiple Dmel Genes in this Orthologous Group
Drosophila melanogaster
fruit fly
Drosophila suzukii
Spotted wing Drosophila
Drosophila simulans
Drosophila sechellia
Drosophila erecta
Drosophila yakuba
Drosophila ananassae
Drosophila pseudoobscura pseudoobscura
Drosophila persimilis
Drosophila willistoni
Drosophila virilis
Drosophila mojavensis
Drosophila grimshawi
Orthologs in non-Drosophila Dipterans (via OrthoDB v9.1) ( EOG091508MA )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Musca domestica
House fly
Musca domestica
House fly
Glossina morsitans
Tsetse fly
Glossina morsitans
Tsetse fly
Lucilia cuprina
Australian sheep blowfly
Lucilia cuprina
Australian sheep blowfly
Mayetiola destructor
Hessian fly
Aedes aegypti
Yellow fever mosquito
Anopheles gambiae
Malaria mosquito
Culex quinquefasciatus
Southern house mosquito
Orthologs in non-Dipteran Insects (via OrthoDB v9.1) ( EOG090W09CN )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Bombyx mori
Silkmoth
Danaus plexippus
Monarch butterfly
Heliconius melpomene
Postman butterfly
Apis florea
Little honeybee
Apis mellifera
Western honey bee
Bombus impatiens
Common eastern bumble bee
Bombus terrestris
Buff-tailed bumblebee
Linepithema humile
Argentine ant
Linepithema humile
Argentine ant
Linepithema humile
Argentine ant
Megachile rotundata
Alfalfa leafcutting bee
Nasonia vitripennis
Parasitic wasp
Nasonia vitripennis
Parasitic wasp
Dendroctonus ponderosae
Mountain pine beetle
Tribolium castaneum
Red flour beetle
Pediculus humanus
Human body louse
Rhodnius prolixus
Kissing bug
Cimex lectularius
Bed bug
Acyrthosiphon pisum
Pea aphid
Zootermopsis nevadensis
Nevada dampwood termite
Orthologs in non-Insect Arthropods (via OrthoDB v9.1) ( EOG090X0NQ0 )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Strigamia maritima
European centipede
Strigamia maritima
European centipede
Strigamia maritima
European centipede
Ixodes scapularis
Black-legged tick
Stegodyphus mimosarum
African social velvet spider
Tetranychus urticae
Two-spotted spider mite
Daphnia pulex
Water flea
Orthologs in non-Arthropod Metazoa (via OrthoDB v9.1) ( EOG091G12OK )
Organism
Common Name
Gene
Multiple Dmel Genes in this Orthologous Group
Strongylocentrotus purpuratus
Purple sea urchin
Ciona intestinalis
Vase tunicate
Ciona intestinalis
Vase tunicate
Gallus gallus
Domestic chicken
Gallus gallus
Domestic chicken
Paralogs
Paralogs (via DIOPT v7.1)
Drosophila melanogaster (Fruit fly) (4)
6 of 10
4 of 10
4 of 10
4 of 10
Human Disease Associations
FlyBase Human Disease Model Reports
Disease Model Summary Ribbon
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Allele
Disease
Evidence
References
Potential Models Based on Orthology ( 0 )
Human Ortholog
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Allele
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease Associations of Human Orthologs (via DIOPT v7.1 and OMIM)
Note that ortholog calls supported by only 1 or 2 algorithms (DIOPT score < 3) are not shown.
Homo sapiens (Human)
Gene name
Score
OMIM
OMIM Phenotype
DO term
Complementation?
Transgene?
Functional Complementation Data
Functional complementation data is computed by FlyBase using a combination of the orthology data obtained from DIOPT and OrthoDB and the allele-level genetic interaction data curated from the literature.
Interactions
Summary of Physical Interactions
Summary of Genetic Interactions
esyN Network Diagram
esyN Network Key:
Suppression
Enhancement

Please look at the allele data for full details of the genetic interactions
Starting gene(s)
Interaction type
Interacting gene(s)
Reference
enhanceable
suppressible
suppressible
suppressible
Starting gene(s)
Interaction type
Interacting gene(s)
Reference
suppressible
External Data
Linkouts
BioGRID - A database of protein and genetic interactions.
DroID - A comprehensive database of gene and protein interactions.
InterologFinder - Protein-protein interactions (PPI) from both known and predicted PPI data sets.
MIST (genetic) - An integrated Molecular Interaction Database
MIST (protein-protein) - An integrated Molecular Interaction Database
Pathways
Gene Group - Pathway Membership (FlyBase)
Epidermal Growth Factor Receptor Ligand Production -
Factors required for the proteolytic cleavage and/or secretion of transforming growth factor-α-like Egfr ligands spi, Krn or grk.
External Data
Linkouts
KEGG Pathways - Wiring diagrams of molecular interactions, reactions and relations.
SignaLink - A signaling pathway resource with multi-layered regulatory networks.
Genomic Location and Detailed Mapping Data
Chromosome (arm)
3L
Recombination map
3-0.5
Cytogenetic map
Sequence location
3L:1,463,811..1,468,944 [+]
FlyBase Computed Cytological Location
Cytogenetic map
Evidence for location
62A2-62A2
Limits computationally determined from genome sequence between P{EP}rhoEP3704&P{PZ}l(3)0622606226 and P{PZ}dlt04276
Experimentally Determined Cytological Location
Cytogenetic map
Notes
References
62A-62A
(determined by in situ hybridisation)
Experimentally Determined Recombination Data
Left of (cM)
Notes
Stocks and Reagents
Stocks (61)
Genomic Clones (21)
cDNA Clones (36)
 

Please Note This section lists cDNAs and ESTs that fall within the genomic extent of the gene model, which may include cDNAs and ESTs of genes within introns, or of overlapping genes. Please see GBrowse for alignment of the cDNAs and ESTs to the gene model.

cDNA clones, fully sequences
BDGP DGC clones
Other clones
Drosophila Genomics Resource Center cDNA clones

For each fully sequenced cDNA the DGRC maintains various forms of the cDNA (e.g tagged or untagged) in several different host vectors for subsequent cloning and expression in Drosophila and Drosophila cell lines.

cDNA Clones, End Sequenced (ESTs)
BDGP DGC clones
RNAi and Array Information
Linkouts
DRSC - Results frm RNAi screens
GenomeRNAi - A database for cell-based and in vivo RNAi phenotypes and reagents
Antibody Information
Laboratory Generated Antibodies
 
polyclonal
Commercially Available Antibodies
 
Other Information
Relationship to Other Genes
Source for database identify of
Source for identity of: rho CG1004
Source for database merge of
Additional comments
Other Comments
rho is not required for patterning of the dorsal anterior follicular epithelium.
rho protein cleaves S within its transmembrane domain.
msk is involved in the nuclear transportation of rho.
rho, sim and vn are required for the formation of the brain lateral to the foregut cells.
dsRNA made from templates generated with primers directed against this gene is tested in an RNAi screen for effects on actin-based lamella formation.
rho protein is localised in the Golgi, where it promotes the cleavage of spi protein.
rho protein appears to be an intramembrane serine protease that directly cleaves spi protein. The putative rho active site is within the membrane bilayer and the spi cleavage site is within its transmembrane domain.
net exhibits a two tiered control in wing vein versus intervein fate by repressing rho transcription and interfering with Egfr signalling downstream of rho.
rho and S function in a synergistic and co-dependent manner, that is independent of spi, to promote vein development through the Egfr/MAPK signalling pathway.
Five EMS induced alleles were identified in a screen for mutations affecting commissure formation in the CNS of the embryo.
rho is required continuously fromm embryonic stage 9-17 to suppress apoptosis in the midline glial (MG) cells. rho may enhance autocrine and paracrine signalling among MG cells.
Candidate gene for quantitative trait (QTL) locus determining bristle number.
The rho NEE enhancer element does not discriminate between TATA-containing and TATA-less promoters.
The differentiation of vein and intervein depends on the outcome of a balance between bs and rho activities, achieved during pupal stages.
Immediately after the movement of the oocyte nucleus to the future dorsal pole a broad activation of the Egfr pathway takes place. As a result, all follicle cells, except the ventral-most rows, express Egfr-target genes. After completion of cell migration, transcription of rho in the dorsal-anterior follicle cells is achieved by activation of the Egfr pathway, in conjunction with signals that may emanate from the anterior, stretch follicle cells. Ectopic activation of rho in the stretch follicle cells can lead to activation of the Egfr pathway in the follicle cells covering the oocyte. Results suggest that rho is responsible for triggering the production or processing of a Egfr ligand that is expressed in the follicle cells.
rho mediates autocrine spi signalling in the follicle cells.
Genetic combinations with mutants of nub cause additive phenotypes.
vvl is required for the specific expression in the tracheal cells of tkv and rho.
In vivo culture of mutant discs from genotypes that are normally embryonic lethal demonstrates rho has no role in wing disc growth.
Clonal analysis suggests salm determines the position of the L2 vein primordium by activating rho expression in neighbouring cells through a locally non-autonomous mechanism. rho then functions to initiate and maintain vein differentiation.
Analysis of rho mutants and targetted rho expression demonstrates the EGF signaling pathway regulates the number of both the dorsal median cells, as well as a set of mesodermal cells that arise next to the midline and express sim.
Study of expression and function of different components of the N pathway in both the wing disc and pupal wings proposes that the establishment of vein thickness utilises a combination of mechanisms. A mechanisms includes repression of rho transcription by HLHmβ and maintenance of Dl expression by rho/Egfr activity.
The function of spi, rho and S appears to be non-autonomous; expression of the precursor only in the midline is sufficient for patterning the ventral ectoderm. Facilitating the expression of spi, rho and S is the only sim-dependent contribution of the midline to patterning the ventral ectoderm, since the mutant sim ectodermal defects can be overcome by expression of secreted spi in the ectoderm. These results suggest a mechanism for generating a graded distribution of secreted spi, which may subsequently give rise to graded activation of Egfr in the ectoderm.
Loss of function mutations in bs are epistatic to loss of function mutations in rho or vn.
The phenotype of a argos null mutant is not observed in a rho mutant background, indicating that rho acts epistatically to argos to regulate the correct number of Ch organs in the embryonic PNS.
The rho protein is concentrated in patches at the apical cell surface. It is possible that rho plaques represent specialized structures defining sites of cell-cell contact at which Egfr signalling is particularly effective.
rho is not required for early expression of sim or vnd in mesectodermal or ventral ectodermal cells, targeted rho expression in embryos results in lateral-to-ventral cell fate shifts in the developing neuroectoderm and midline targeted rho expression can rescue the medial denticle fusion in rho mutant cuticles.
Mutations of rho enhance penetrance of ectopic crossveins in chicgdh-5/EgfrE1 heterozygotes.
Molecular analysis suggests that sna protein acts over distances of 50-150bp to block the activity, but not the binding, of the dl activator to the rho 650bp enhancer.
The spi product triggers the Egfr signaling cascade. Graded activation of the Egfr pathway may normally give rise to a repertoire of discrete cell fates in the ventral ectoderm and graded distribution of spi may be responsible for the graded activation. The rho and S products may act as modulators of Egfr signaling. Epistatic relationships suggest that rho and S may normally facilitate processing of the spi precursor.
Ectopic expression of both rho and Dl in a mutant net background produces ectopic veins of normal thickness. Ectopic expression of rho alone produces whole intervein sectors converted into vein. The pattern of normal+ectopic wing veins resembles wing vein patterns of other flies with more veins than Drosophila.
Double mutant genetic clones with vn have extreme nonautonomous effects in the proliferation of wild type cells in the wing.
Dorsal-ventral patterning is regulated by a signalling pathway that includes Tl and transcription factors, dl, that interact with related enhancers, rho. The κ enhancer from mouse is capable of generating lateral stripes of Ecol\lacZ gene expression in transgenic embryos in a pattern similar to that directed by rho enhancer. Results suggest that enhancers can couple conserved signalling pathways to divergent gene functions, dorso-ventral patterning and mammalian haematopoiesis.
A single sna-binding site in the rho promoter region can mediate repression of rho.
Enhancer piracy lines reveal an unanticipated role for rho in imaginal disc formation and provide evidence that mis-expression of rho is sufficient for converting entire intervein sectors into veins.
Mutation in rho affects sensory organ precursor formation.
rho is required for PNS development in the embryo.
The differentiation of individual mesectoderm cells (MECs) lineages is traced. rho is necessary for determining the correct number of cells in many neuronal MEC lineages. The correct number of midline glia are determined but later become apoptotic in embryos mutant for rho.
rho is involved in the downregulation of Egfr mRNA.
Analysis of mutant embryos determines that growth cones can distinguish between individual muscle fibres during synaptogenesis. Growth cones retain their target preference even when the numbers and patterns of muscle fibres are altered.
The E boxes within the neural ectoderm expression enhancer region (NEE) play a role in neuroectoderm gene expression.
Promoter fusions using elements of the twi, ve, da and sna promoters indicate that low affinity dl-binding sites restrict target gene expression to the presumptive mesoderm, where there are peak levels of dl expression, while high affinity sites in other target genes permit expression in ventrolateral regions where dl levels are intermediate. Activation by low levels of dl in lateral regions depends on cooperative interaction between dl and other basic helix loop helix proteins. Promoters containing the Et (veinlet) or Eds (dl and snail) E boxes display opposite behaviour in da and twi mutants, suggesting they are regulated by different basic helix loop helix proteins.
The gene product is localized on the apical surface of the dorsal-anterior follicle cells surrounding the oocyte. Loss of function mutations cause ventralization of the egg shell and embryo, whereas ectopic expression leads to their dorsalization. Double mutant analysis indicates that rho acts upstream of Toll in dorsal-ventral axis formation, and the action of rho requires the grk-Egfr signaling pathway. rho expression pattern in embryogenesis is altered in fs(1)K10 mutants.
A H{Lw2} insertion at cytological location 62A (line 79) is viable and causes a recessive rough eye phenotype. The H{Lw2} element may have inserted into a gene adjacent to rho causing the rough eye phenotype and is responding to rho enhancer elements or the insertion may be into the rho gene causing an undescribed eye phenotype.
rho is likely to be the earliest known gene to be expressed in the longitudinal wing vein primordia and the rho continues to be expressed in developing wing veins during the partitioning of the wing into vein versus intervein areas.
Role of rho in eye development studied: whereas mutant clones in the eye have only a subtle phenotype, ectopic expression of rho causes non-neural mystery cells to be transformed into photoreceptors.
Expression of rho is blocked in ventral regions by sna. A neural ectoderm expression region (NEE) of 300bp has been defined in the rho promoter, and contains a cluster of dl and basic HLH activator sites closely linked to a sna repressor sites. Mutations in these sites cause predicted changes in the level of expression. Similarity of this system to eve stripe 2 suggests dl and bcd use similar mechanisms to generate their respective stripes.
rho gene product is required for the proper development of the ventralmost cuticle and the CNS midline.
Basic protein structure, comparison of phenotypes and spatial and temporal expression patterns suggest that spi encodes a ligand that functionally interacts with the products of rho and possibly Egfr.
sim gene product is required for the normal expression of rho.
Zygotically active locus involved in the terminal developmental program in the embryo.
Mutations lead to ventrolateral pattern defects and peripheral nervous system abnormalities.
rho is involved in the elaboration of positional information at a ventrolateral level in the embryo. rho acts very early in differentiation pathways to specify the identities of domains and isolated precursor cells. rho, pnt, S and spi all function in the formation of the same chordotonal organs.
Mutations in rho cause pleiotropic phenotypes in embryonic patterns and affect several longitudinal veins.
ve, vn, ci, cg, svs, ast, H, Vno and vvl belong to the vein phenotypic group (Puro, 1982, Droso. Info. Serv. 58:205--208 ) within the 'lack-of-vein' mutant class. Loss-of-function alleles at these loci remove stretches of veins in two or more longitudinal veins. Double mutations within members of this group remove all veins, have smaller, slightly lanceolate wings, no sensilla and extra chaetae. Some alleles are embryonic lethal.
rho mutants display a pointed head skeleton and deletion of the medial portion in all denticle belts.
Viable alleles exhibit wing venation defects; strong alleles are embryonic lethal. In flies homozygous for viable alleles the L3, L4 and L5 veins do not reach the wing margins (Duncan, 1935; Waddington, 1939). Developmentally, veins appear complete in prepupa but distal tips are obliterated during the contraction period (Waddington, 1939; Waddington, 1940). The shortened-vein phenotype is suppressed by px1 (Waddington), net1, and su(ve)1 and is enhanced by vn1, H1, NAx-1, ci1, tg2 and kniri-1 (Waddington; Diaz-Benjumea and Garcia-Bellido, 1990). Vein-specific modifiers, such as gp1, (Bridges and Morgan, 1919) or PL(2)L4 (Thompson, 1976), interact with the effect of rhove-1 on L4. The L5 vein seldom extends beyond the posterior crossvein. rhove-2 is a stronger allele, in which the L2 is also affected (Bertschmann); L2 vein occasionally complete (Thompson, 1976), but other veins do not overlap wild type. Distribution of sense organs (campaniform sensilla and bristles) on L3 is shifted proximally in rhove-1 (Spivey and Thompson, 1984) When a rhove-1 stock is selected for shortened veins, the F1 produced by mating wild-type males to mutant females show terminal gaps in L5 (Thompson and Thoday, 1976). rhove-1/rhove-1/+ intersexes are veinlet, whereas rhove-1/rhove-1/+ triploids are normal, according to Pipkin. Interestingly flies heterozygous for rhove-1 and strong embryonic lethal alleles display less severe veinlet phenotypes than rhove-1 homozygotes (Bier, Jan and Jan, 1990; Diaz-Benjumea and Garcia-Bellido, 1990); furthermore, rhove-1/rho5 flies appear wild type (Bier, unpublished). Homozygous rho5 embryos exhibit three major types of defects: (1) Dorsoventral defects: Embryos exhibit a deletion of epithelial cells derived from a ventrolateral strip of the blastoderm fate map (i.e., loss of mediolateral cuticular denticles and sensory structures). Other phenotypes resulting from blastoderm patterning defects include failure to complete dorsal closure and development of an abnormal pointed head skeleton (Jurgens et al., 1984; Mayer and Nusslein-Volhard, 1988). (2) Midline defects: Mesectodermal cells giving rise to glia and unpaired neurons are abnormal or fail to form. Late developmental consequences include a narrower CNS and pathfinding abnormalities (Mayer and Nusslein-Volhard, 1988). (3) Peripheral-nervous-system defects: Two stretch receptor organs (lateral abdominal chordotonal organs) fail to form in lethal rhove-1 mutants. The primary chordotonal-organ-precursor cells are likely to be affected since the four progeny sensory-organ cells derived from that precursor cell are missing as a group (Bier, Jan and Jan, 1990). Other late embryonic defects include loss of longitudinal body-wall muscles, ventrally displaced muscle-attachment sites (Bier, Jan and Jan, 1990) and loss of the first row of denticles in abdominal segments (Mayer and Nusslein-Volhard, 1988).
Origin and Etymology
Discoverer
Etymology
Identification
External Crossreferences and Linkouts ( 43 )
Sequence Crossreferences
NCBI Gene - Gene integrates information from a wide range of species. A record may include nomenclature, Reference Sequences (RefSeqs), maps, pathways, variations, phenotypes, and links to genome-, phenotype-, and locus-specific resources worldwide.
GenBank Nucleotide - A collection of sequences from several sources, including GenBank, RefSeq, TPA, and PDB.
GenBank Protein - A collection of sequences from several sources, including translations from annotated coding regions in GenBank, RefSeq and TPA, as well as records from SwissProt, PIR, PRF, and PDB.
RefSeq - A comprehensive, integrated, non-redundant, well-annotated set of reference sequences including genomic, transcript, and protein.
UniProt/Swiss-Prot - Manually annotated and reviewed records of protein sequence and functional information
UniProt/TrEMBL - Automatically annotated and unreviewed records of protein sequence and functional information
Other crossreferences
BDGP expression data - Patterns of gene expression in Drosophila embryogenesis
Drosophila Genomics Resource Center - Drosophila Genomics Resource Center (DGRC) cDNA clones
Eukaryotic Promoter Database - A collection of databases of experimentally validated promoters for selected model organisms.
Fly-FISH - A database of Drosophila embryo and larvae mRNA localization patterns
Flygut - An atlas of the Drosophila adult midgut
GenomeRNAi - A database for cell-based and in vivo RNAi phenotypes and reagents
InterPro - A database of protein families, domains and functional sites
KEGG Genes - Molecular building blocks of life in the genomic space.
KEGG Pathways - Wiring diagrams of molecular interactions, reactions and relations.
modMine - A data warehouse for the modENCODE project
SignaLink - A signaling pathway resource with multi-layered regulatory networks.
Linkouts
BioGRID - A database of protein and genetic interactions.
DPiM - Drosophila Protein interaction map
DroID - A comprehensive database of gene and protein interactions.
DRSC - Results frm RNAi screens
FLIGHT - Cell culture data for RNAi and other high-throughput technologies
FlyAtlas - Adult expression by tissue, using Affymetrix Dros2 array
FlyMine - An integrated database for Drosophila genomics
Interactive Fly - A cyberspace guide to Drosophila development and metazoan evolution
InterologFinder - Protein-protein interactions (PPI) from both known and predicted PPI data sets.
KEGG Pathways - Wiring diagrams of molecular interactions, reactions and relations.
MIST (genetic) - An integrated Molecular Interaction Database
MIST (protein-protein) - An integrated Molecular Interaction Database
Synonyms and Secondary IDs (31)
Reported As
Symbol Synonym
rho
(Jia et al., 2019, Meltzer et al., 2019, Zandvakili et al., 2019, Zhang et al., 2019, Duan et al., 2018, Garrido-Jimenez et al., 2018, Kavaler et al., 2018, Kittelmann et al., 2018, Ogura et al., 2018, Qin et al., 2018, Schwarz et al., 2018, Chambers et al., 2017, Osterfield et al., 2017, Ozasa et al., 2017, Revaitis et al., 2017, Rogers et al., 2017, Tomita et al., 2017, Wang et al., 2017, Crocker et al., 2016, Fukaya et al., 2016, Jussen et al., 2016, Malartre, 2016, Sarov et al., 2016, Testa and Dworkin, 2016, Dahlberg et al., 2015, He et al., 2015, Lim et al., 2015, Matsuda et al., 2015, Matsuda et al., 2015, Yurgel et al., 2015, Austin et al., 2014, Fauré et al., 2014, Fu et al., 2014, Mannervik, 2014, Rembold et al., 2014, Shimamura et al., 2014, Taylor et al., 2014, Valentine et al., 2014, Cheung et al., 2013, Curtis et al., 2013, Dresch et al., 2013, Garcia et al., 2013, Hong et al., 2013, Külshammer and Uhlirova, 2013, McKay and Lieb, 2013, Molnar and de Celis, 2013, Osterfield et al., 2013, Peters et al., 2013, Robinson and Atkinson, 2013, Rougeot et al., 2013, Saunders et al., 2013, Sopko and Perrimon, 2013, Steinhauer et al., 2013, Webber et al., 2013, Butchar et al., 2012, Haskel-Ittah et al., 2012, Hudry et al., 2012, Japanese National Institute of Genetics, 2012.5.21, Li-Kroeger et al., 2012, Maeng et al., 2012, Nagel et al., 2012, Niepielko et al., 2012, Rushlow and Shvartsman, 2012, Simakov et al., 2012, Stinchfield et al., 2012, Ajuria et al., 2011, Cernilogar et al., 2011, Cherbas et al., 2011, Dworkin et al., 2011, Fay et al., 2011, Hogan et al., 2011, Hwang and Rulifson, 2011, Jiang et al., 2011, Kawamori et al., 2011, Lynch and Roth, 2011, Moses et al., 2011, Mouchel-Vielh et al., 2011, Mrinal et al., 2011, Murillo-Maldonado et al., 2011, Ozdemir et al., 2011, Pilgram et al., 2011, Tjota et al., 2011, Wojcinski et al., 2011, Bothma et al., 2010, Castoreno et al., 2010, Crocker et al., 2010, Fakhouri et al., 2010, Figeac et al., 2010, Gutzwiller et al., 2010, Jones et al., 2010, Klein et al., 2010, Morozova et al., 2010, Rendina et al., 2010, Rousso et al., 2010, Tipping et al., 2010, Uhl et al., 2010, Wang et al., 2010, Witt et al., 2010, Yasugi et al., 2010, Yogev et al., 2010, Yu et al., 2010, Birkholz et al., 2009, Birkholz et al., 2009, Boettiger and Levine, 2009, Debat et al., 2009, Huh et al., 2009, Jiang and Edgar, 2009, Krejcí et al., 2009, Lachance et al., 2009, Mao and Freeman, 2009, Marco et al., 2009, Maybeck and Röper, 2009, Papatsenko et al., 2009, Yan et al., 2009, Zartman et al., 2009, Beaver et al., 2008, Duong et al., 2008, Gebelein et al., 2008, Gilchrist et al., 2008, Haecker et al., 2008, Iyadurai et al., 2008, Kagesawa et al., 2008, Li et al., 2008, Li-Kroeger et al., 2008, McNeill et al., 2008, Qi et al., 2008, Ratnaparkhi et al., 2008, Yakoby et al., 2008, Yakoby et al., 2008, Zartman et al., 2008, Astigarraga et al., 2007, Beltran et al., 2007, Bonds et al., 2007, Buszczak et al., 2007, Escudero et al., 2007, Foltenyi et al., 2007, Georlette et al., 2007, Halfon and Arnosti, 2007, Kim et al., 2007, Li et al., 2007, Lilja et al., 2007, Maeda et al., 2007, Muse et al., 2007, Muse et al., 2007, Nishimura et al., 2007, Ruel et al., 2007, Sandmann et al., 2007, Zeitlinger et al., 2007, Zeitlinger et al., 2007, Zeitlinger et al., 2007, Atkey et al., 2006, Biemar et al., 2006, Brodu and Casanova, 2006, Brown et al., 2006, Cela and Llimargas, 2006, Chanut-Delalande et al., 2006, Charroux et al., 2006, Dworkin and Gibson., 2006, Guichard et al., 2006, Hashimoto and Yamaguchi, 2006, Kim et al., 2006, Laplante and Nilson, 2006, Lawrence, 2006, Liu et al., 2006, Miura et al., 2006, Molnar et al., 2006, Mukherjee et al., 2006, Oishi et al., 2006, Pallavi et al., 2006, Parker, 2006, Zinzen et al., 2006, Zinzen et al., 2006, Galindo et al., 2005, Jordan et al., 2005, Reeves and Posakony, 2005, Ruiz-Gomez et al., 2005, Sotillos and De Celis, 2005, Stathopoulos and Levine, 2005, Angulo et al., 2004, Kim et al., 2004, Markstein et al., 2004, Chang et al., 2003, Cowden and Levine, 2003, Lee et al., 2002, Chang et al., 2001, DeLotto, 2001, Hewitt et al., 1999, Lee et al., 1999)
rhomboid/veinlet
Name Synonyms
RHOMBOID
Veinlet
rhomboid
(Osterfield et al., 2017, Tomita et al., 2017, Wang et al., 2017, Crocker et al., 2016, Fukaya et al., 2016, Jussen et al., 2016, Malartre, 2016, Wieschaus and Nüsslein-Volhard, 2016, Dahlberg et al., 2015, Kohlmaier et al., 2015, Legent et al., 2015, Matsuda et al., 2015, Matsuda et al., 2015, Austin et al., 2014, Rembold et al., 2014, Zhang et al., 2014, Hahn et al., 2013, Hong et al., 2013, McKay and Lieb, 2013, Molnar and de Celis, 2013, Rougeot et al., 2013, Bryantsev et al., 2012, Haskel-Ittah et al., 2012, Hudry et al., 2012, Maeng et al., 2012, Nagel et al., 2012, Pearson et al., 2012, Stinchfield et al., 2012, Ajuria et al., 2011, Jiang et al., 2011, Moses et al., 2011, Murillo-Maldonado et al., 2011, Urban and Dickey, 2011, Biehs et al., 2010, Buchon et al., 2010, Fakhouri et al., 2010, Figeac et al., 2010, Jones et al., 2010, Li et al., 2010, Lin et al., 2010, Morozova et al., 2010, Witt et al., 2010, Birkholz et al., 2009, Birkholz et al., 2009, Chung et al., 2009, Corl et al., 2009, Hurlbut et al., 2009, Jiang and Edgar, 2009, Krejcí et al., 2009, Terriente-Félix and de Celis, 2009, Yan et al., 2009, Berger et al., 2008, Crocker et al., 2008, Haecker et al., 2008, Li et al., 2008, Li-Kroeger et al., 2008, Qi et al., 2008, Ratnaparkhi et al., 2008, Astigarraga et al., 2007, Baker et al., 2007, Bonds et al., 2007, Chen et al., 2007, Escudero et al., 2007, Foltenyi et al., 2007, Grueber et al., 2007, Li et al., 2007, Lilja et al., 2007, Lin et al., 2007, Maeda et al., 2007, Nibu et al., 2007, Nishimura et al., 2007, Nishimura et al., 2007, O'Keefe et al., 2007, Tadros et al., 2007, Atkey et al., 2006, Biemar et al., 2006, Dworkin and Gibson, 2006, Guichard et al., 2006, Kim et al., 2006, Oishi et al., 2006, Parker, 2006, Urban, 2006, Ward et al., 2006, Galindo et al., 2005, Jordan et al., 2005, Melen et al., 2005, Ruiz-Gomez et al., 2005, Sotillos and De Celis, 2005, Takaesu et al., 2005, Kim et al., 2004, Markstein et al., 2004, Voas and Rebay, 2004, Cowden and Levine, 2003, Nibu et al., 2003, Pribyl et al., 2003, Chang et al., 2001, DeLotto, 2001, Lee et al., 1999)
Secondary FlyBase IDs
  • FBgn0003251
  • FBgn0003972
  • FBgn0026834
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Study focus (0)
Experimental Role
Project
Project Type
Title
References (934)