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General Information
Symbol
Dmel\Ras85DΔC40B
Species
D. melanogaster
Name
FlyBase ID
FBal0083262
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Ras1ΔC40b, RasΔC40b, rasC40B, rasD40
Mutagen
    Nature of the Allele
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference
    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 ( 1 )
    Disease
    Interaction
    References
    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
     
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In
    Detailed Description
    Statement
    Reference
    Type II neuroblast lineage MARCM clones mutant for Ras85DΔC40B do not display any significant changes in the clone morphology, size or the number of progenitor cells it contains compared to wild-type clones.
    Although the initial growth of Ras85DΔC40B mutant intestinal stem cell clones is normal, their long-term proliferation is severely compromised. These clones do not grow even after the flies have recovered from Pseudomonas entomophila infection.
    6 days after clone induction, 100% of testes carry one or more marked homozygous CPC clones, with an average of 3.4 marked homozygous CPCs per testis (compared to 92% of testes carrying one or more marked wild-type CPC clones, with an average of 1.1 marked wild-type CPCs per testis).
    Ras85DΔC40B mutant eye disc clones show defects in ommatidium development. Gaps and partially-formed rosettes are observed within the ommatidial array.
    In Ras85DΔC40B mutant adult Malpighian tubule clones only a few differentiated renalcytes (RCs) are detected, reduced in number compared to control clones.
    Homozygous Ras85DΔC40B mutant adult midgut progenitor cells fail to proliferate during larval development.
    Homozygous clones in the eye disc are much smaller than their wild-type twin spots.
    Ras85DΔC40B 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.
    Larval eye discs containing Ras85DΔC40B clones show a higher level of cell death than controls.
    Clones of Ras85DΔC40B generated in the developing eye are aberrantly small.
    Oocyte polarity and apical-basal polarity of posterior follicle cells (PFCs) is disrupted in Ras85DΔC40B mutant PFC clones.
    The initiation of mesoderm spreading is unaffected in homozygous embryos derived from homozygous female germline clones.
    Embryos derived from homozygous Ras85DΔC40B female germ line clones have 20-30% fewer pole cells by the cellularization stage, due to mitotic defects, when compared with wild-type embryos. These mutant embryos exhibit defective gastrulation and lack the posterior midgut primordium. The majority of pole cells are unable to enter the embryo at gastrulation and those that do enter the embryo appear abnormal in both directed migration and aggregation, leading to their random scattering in the embryonic cavity. Analysis of pole cell transplantations, in which pole cells from cellularization stage embryos derived from Ras85DΔC40B female germ line clones and wild-type fathers are transplanted into wild-type embryos shows that no Ras85DΔC40B pole cells are ever found in the gonad of the transplanted embryo but migrate to ectopic locations. These Ras85DΔC40B mutant pole cells disappear in late stage embryos, possibly due to cell death.
    In Ras85DΔC40B mutant somatic clones in the 3rd instar eye disc, photoreceptors R2-R5 fail to undergo or differentiation. Within Ras85DΔC40B mutant somatic clones there is a failure of G1 arrest in the furrow: all cells except R8s re-enter the cell cycle. However, none of these cells progress past G2.
    Homozygous clones in the follicle cells are smaller than control clones and are detected at a lower frequency 6 days after clone induction. Large follicle stem cell clones are not recovered 10 days after clone induction. 16% of stage 14 eggshells laid by mosaic females (containing homozygous follicle cell clones) 5-7 days after clone induction have dorsal appendage defects. The defects include complete lack of dorsal appendages (15%), a small "nub" of extra chorion material next to two normal dorsal appendages (4.5%), short dorsal appendages (11%), fragmented dorsal appendages (11%), one dorsal appendage replaced by a nub of chorion material (42%), both dorsal appendages replaced by a nub of chorion material (12%) and fragmented dorsal appendages plus an extra nub of material (4.5%). Mutant cells are not found amongst the migrating follicle cells that give rise to dorsal appendages. Aberrant nubs and fragments of dorsal appendages are not made by mutant cells, but by wild-type cells adjacent to mutant clones. Egg chambers with dorsal anterior mutant clones show gross disruption of the apical morphology of the dorsal appendage primordia at stage 12.
    Homozygous somatic clones in the wing, autonomously prevent wing vein formation.
    Homozygous embryos show loss of VA2 muscle precursor cells (only 9% of hemisegments contain VA2 precursor cells).
    Excess R8 cell precursors are seen in homozygous clones in the eye disc.
    A gradual decline over time in the number of homozygous clones present compared to wild-type sister clones is seen in imaginal discs. There is also a decline in the area of the surviving homozygous clones compared to wild-type clones. The homozygous clones contain many pyknotic nuclei. Relatively large homozygous clones containing 40-80 cells are seen even 72 hours after induction, but at a low frequency. Homozygous clones (which are RpS3+) induced in discs which are RpS3-/+ have increased survival rates and are larger than homozygous clones induced in a wild-type background.
    Embryos derived from homozygous female germline clones develop abdominal segment A8 in 20.3% of cases and filzkorper in 0.4% of cases.
    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Enhanced by
    Statement
    Reference
    Suppressed by
    Enhancer of
    Statement
    Reference
    NOT Enhancer of
    Suppressor of
    NOT Suppressor of
    Statement
    Reference
    Other
    Phenotype Manifest In
    Enhanced by
    Statement
    Reference
    Suppressed by
    NOT suppressed by
    Enhancer of
    Statement
    Reference
    Ras85DΔC40B is an enhancer of phenotype of cswlf
    Ras85DΔC40B is an enhancer of eye phenotype of hidGMR.PG/WGMR.PG
    NOT Enhancer of
    Statement
    Reference
    Ras85DΔC40B is a non-enhancer of eye phenotype of upd1GMR.PB
    Suppressor of
    Statement
    Reference
    NOT Suppressor of
    Statement
    Reference
    Ras85DΔC40B is a non-suppressor of eye phenotype of upd1GMR.PB
    Ras85DΔC40B is a non-suppressor of phenotype of Src42ASu(Raf)1-1
    Other
    Additional Comments
    Genetic Interactions
    Statement
    Reference
    The reduced number of progenitor cells in cnoR2 clones is not significantly affected by combination with Ras85DΔC40B, but the morphology and size of the clones and the neuroblasts within them is more similar to wild-type.
    Ras85DΔC40B, Stat92E397 double mutant intestinal stem cell clones are smaller than adjacent cells and lack enterocyte cells.
    Ras85DΔC40B, scrib1 double mutant adult Malpighian tubule clones display only a few differentiated renalcytes (RCs), like the single Ras85DΔC40B mutant phenotype. Ras85DΔC40B, sav3 double mutant adult Malpighian tubule clones display only a few differentiated renalcytes (RCs), like the single Ras85DΔC40B mutant phenotype.
    Ras85DΔC40B, cicQ474X double mutant clones in the eye disc are typically larger than their wild-type twin spots, as occurs in cicQ474X single mutant clones. In the adult, double mutant clones are seen, but the mutant tissue lacks the normal ommatidial architecture. Ras85DΔC40B Tsc1unspecified double mutant clones in the eye discs are no larger than Ras85DΔC40B single mutant clones.
    Expressing atoScer\UAS.cJa under the control of Scer\GAL4GMR.PF fails to suppress the morphogenetic furrow phenotype of Ras85DΔC40B clones.
    Larval eye discs containing Ras85DΔC40B, RassfX36 double mutant clones show a partial rescue of the increased cell death phenotype observed in discs with Ras85DΔC40B single mutant clones.
    Double-mutant Ras85DΔC40B, RassfX36 clones in the eye show a rescue of the growth defect seen in single mutant Ras85DΔC40B clones.
    The oocyte polarity defects seen when Ras85DΔC40B mutant clones are made in the posterior follicle cell layer are partially rescued by expression of DgdsRNA.Scer\UAS in the clone using Scer\GAL4Act and the 'MARCM' technique. The polarity defects of posterior follicle cells (PFCs) seen in Ras85DΔC40B mutant PFC clones are partially rescued by expression of DgdsRNA.Scer\UAS in the clone using Scer\GAL4Act and the 'MARCM' technique.
    Neural differentiation and the second mitotic wave are blocked in clones of cells in the eye disc simultaneously mutant for DlRevF10 and Ras85DΔC40B in a Minute/+ background: mutant cells in the position of the second mitotic wave do not enter S phase and do not undergo mitosis, as in DlRevF10 clones.
    Embryos derived from double mutant Stat92E06346; Ras85DΔC40B female germ line clones have 54% fewer pole cells by the cellularization stage than wild-type embryos, which is a greater reduction than is seen in embryos derived from either single mutant female germline clone. Pole cells of these double mutant embryos appear slighlty larger than wild-type cells, consistent with their slower mitotic division rate.
    Within Ras85DΔC40B mutant clones in the eye disc in a BacA\p35GMR.PH background, caspase activation is seen posterior to column 5, relative to the morphogenetic furrow. There is no increase in caspase activation outside of these clones.
    The addition of cicD49 suppresses the loss of wing vein phenotype seen in Ras85DΔC40B clones.
    Expression of csw::Src64Bsrc90.Scer\UAS under the control of Scer\GAL4twi.PG partially suppresses the loss of VA2 muscle precursor cells seen in Ras85DΔC40B embryos (21% of hemisegments have VA2 cells).
    Expression of BacA\p35Scer\UAS.cHa under the control of Scer\GAL4en-e16E increases the survival of homozygous Ras85DΔC40B clones in the imaginal disc from 2% to 86% (at 72 hours after induction of the clone). The size of the clones is also increased compared to their wild-type sister clones, although there is still a large size difference between them.
    A higher proportion of embryos derived from homozygous female germline clones develop abdominal segment A8 (52.9%) or filzkorper (12.4%) if the females are also carrying Src42A7-4.
    Does not suppress the ability of Src42ASu(phl)1-1 to suppress the lethality of phl1/Y flies.
    Embryos derived from phlSu3, Ras85DΔC40B double mutant germ cells die during embryogenesis with cuticles indistinguishable from those of Ras85DΔC40B mutants.
    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Comments
    Expression of Ras85DScer\UAS.cKa under the control of Scer\GAL4αTub84B.PL in combination with Scer\GAL80ts.αTub84B in eye disc clones rescues the ommatidial development defects of Ras85DΔC40B homozygous cells. Expression of Ras85DKtail.Scer\UAS.T:Hsap\CAAX.T:Hsap\MYC under the control of Scer\GAL4αTub84B.PL in combination with Scer\GAL80ts.αTub84B in eye disc clones can partially rescue the ommatidial development defects of Ras85DΔC40B homozygous cells. Expression of Ras85DK187V.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4αTub84B.PL in combination with Scer\GAL80ts.αTub84B in eye disc clones can partially rescue the ommatidial development defects of Ras85DΔC40B homozygous cells. Expression of Ras85DKtail6Q.Scer\UAS.T:Hsap\MYC.T:Hsap\CAAX-6Q under the control of Scer\GAL4αTub84B.PL in combination with Scer\GAL80ts.αTub84B in eye disc clones can partially rescue the ommatidial development defects of Ras85DΔC40B homozygous cells. Expression of Ras85DC186S.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4αTub84B.PL in combination with Scer\GAL80ts.αTub84B in eye disc clones rescues the ommatidial development defects of Ras85DΔC40B homozygous cells. Clones show an enhanced recruitment of supernumerary photoreceptor cells. Expression of Ras85DV12.Scer\UAS under the control of Scer\GAL4αTub84B.PL in combination with Scer\GAL80ts.αTub84B in eye disc clones rescues the ommatidial development defects of Ras85DΔC40B homozygous cells. Clones show hyper-recruitment of photoreceptors. Expression of Ras85D12V,C186S.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4αTub84B.PL in combination with Scer\GAL80ts.αTub84B in eye disc clones rescues the ommatidial development defects of Ras85DΔC40B homozygous cells. Clones show an enhanced recruitment of supernumerary photoreceptor cells.
    The size and survival of homozygous Ras85DΔC40B clones in the imaginal disc is completely rescued by expression of Ras85DScer\UAS.cKa under the control of Scer\GAL4en-e16E.
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    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (24)
    References (41)