ve, Rho1, rhomboid-1, rho-1, veinlet
serine protease - transmembrane protein involved with Epidermal growth factor receptor signaling - required for the production or processing of Spitz, the Egfr ligand
Please see the GBrowse view of Dmel\rho or the JBrowse view of Dmel\rho for information on other features
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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
2.9, 2.5 (northern blot)
355 (aa); 39 (kD)
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.
Comment: 25-30 hr APF
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as procephalic ectoderm anlage in statu nascendi
Comment: reported as pericardial cell specific anlage
Comment: reported as posterior spiracle specific anlage
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 expression is first observed in the leg disc at 86 hr AEL in a central domain and in concentric rings. Expression is weak until 96 hr AEL at which point the central domain is substituted by a small cluster of cells in the ventral pretarsus, in the pit of cells that give rise to the tendon. The concentric rings of expression are located in the presumptive tibea, tibia/femur boundary, and trochanter positions. By 120 hr AEL, the doral femoral cluster has become a twin cluster and there is now a ring in every presumptive leg segment. Pretarsal expression has disappeared. This pattern persists at 8 hr APF, when the rings of expression can be seen as stripes in the everted leg with additional isolated expressing cells in the pretarsus. Each rho stripe saddles the fold between adjacent segments, and has a graded intensity, which is weaker proximally and stronger distally.
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.
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.
GBrowse - Visual display of RNA-Seq signals
View Dmel\rho in GBrowse 23-0.5
Please Note FlyBase no longer curates genomic clone accessions so this list may not be complete
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.
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.
polyclonal
monoclonal
Source for identity of: rho CG1004
rho is not required for patterning of the dorsal anterior follicular epithelium.
dsRNA made from templates generated with primers directed against this gene is tested in an RNAi screen for effects on actin-based lamella formation.
Five EMS induced alleles were identified in a screen for mutations affecting commissure formation in the CNS of the embryo.
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.
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.
Genetic combinations with mutants of nub cause additive phenotypes.
In vivo culture of mutant discs from genotypes that are normally embryonic lethal demonstrates rho has no role in wing disc growth.
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.
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.
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.
Mutation in rho affects sensory organ precursor formation.
rho is required for PNS development in the embryo.
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.
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.
Zygotically active locus involved in the terminal developmental program in the embryo.
Mutations lead to ventrolateral pattern defects and peripheral nervous system abnormalities.
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).
