Allele Dmel\rho7M43
| General Information | |||
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| Symbol | Dmel\rho7M43 | Species | D. melanogaster |
| Name | FlyBase ID | FBal0017858 | |
| Feature type | allele | Associated gene | Dmel\rho |
| Also Known As | rho7M, ve4 | ||
| Allele class | amorphic allele - genetic evidence | ||
| Mutagen | ethyl methanesulfonate | ||
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| Description |
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| FB2013_03 | |||
| FB2013_02 | |||
| All updates | Click here to see a list of all updates to this record from FB2010_08 and on. | ||
Nature of the Allele
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| Allele class | |||
| Mutagen | |||
| Mutations Mapped to the Genome | |||
Type Location Additional Notes References | |||
| Associated Sequence Data | |||
| DDBJ
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EMBL / GenBank | DNA sequence Protein sequence Name | ||
| UniProtKB/Swiss-Prot | |||
| UniProtKB/TrEMBL | |||
| Progenitor genotype | |||
| Nature of the lesion | Statement Reference | ||
| Cytology | |||
Phenotypic Data
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Phenotypic Class
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Phenotype Manifest In
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larval sense organ & antennal segment larval sense organ & maxillary segment | |||
Detailed Description
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Statement Reference R8 differentiation is defective in rho[7M43] 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 rho[7M43] 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. 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
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| Linkouts | |||
Interactions
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Phenotypic Class
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Enhanced by | |||
Statement Reference | |||
Enhancer of | |||
Statement Reference | |||
NOT Enhancer of | |||
Statement Reference | |||
Suppressor of | |||
Statement Reference vn[+], vn1, rho7M43, rho[+] is a suppressor | partially of visible phenotype of tumΔE1E.Scer\UAS, Scer\GAL4en-e16E | |||
Other | |||
Statement Reference | |||
Phenotype Manifest In
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Enhanced by | |||
Statement Reference rho7M43 has photoreceptor cell R8 | somatic clone | cell non-autonomous phenotype, enhanceable by ru1 | |||
Enhancer of | |||
Statement Reference rho7M43 is an enhancer of photoreceptor cell R8 | somatic clone | cell non-autonomous phenotype of ru1 | |||
Suppressor of | |||
Statement Reference rho7M43/rho[+] is a suppressor of phenotype of Src42ASu(phl)1-1 rho7M43/rho+ is a suppressor of wing vein | ectopic phenotype of Scer\GAL4tub.PU, cswN308D.Scer\UAS.P\T vn[+], vn1, rho7M43, rho[+] is a suppressor | partially of wing phenotype of tumΔE1E.Scer\UAS, Scer\GAL4en-e16E | |||
Other | |||
Statement Reference | |||
Additional Comments
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Genetic Interactions
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Statement Reference 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. 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
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Statement Reference | |||
Complementation & Rescue Data
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| Fails to complement | |||
| Partially rescued by | |||
| Comments | rho[Scer\UAS.cGa] driven by Scer\GAL4[rho.654] rescues the oenocyte defect but not the secondary sensory organ precursor cell defects associated with rho[7M43]. | ||
Stocks
( 1 ) | |||
| Bloomington | |||
Notes on Origin
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| Discoverer | Jurgens. | ||
Associated with: ru1. | |||
Comments
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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 & Linkouts
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| Other Crossreferences | |||
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Synonyms & Secondary IDs
( 14 ) | |||
| Reported As | |||
| Symbol Synonym | rho17M43 rho-17M43 rho7M3 rho7M43 rho7m43 rho7M rho7m rhove-4 rhomboid7M43 rhomboid7M ve4 ve7M43 | ||
| Name Synonym | rhomboid7M43 | ||
| Secondary FlyBase IDs | |||
References
( 53 ) | |||
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Recent research papers ( 1 ) | |||
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Recent Updates
External Crossreferences & Linkouts