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General Information
Symbol
Dmel\SerRX106
Species
D. melanogaster
Name
FlyBase ID
FBal0030221
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Mutagen
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Cytology

Polytene chromosomes normal.

Nature of the lesion
Statement
Reference

Exon 6 and part of exon 7 are deleted.

Internal deletion of 9kb of the transcribed region.

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

denticle row 3 & abdominal 2 ventral denticle belt

denticle row 3 & abdominal 3 ventral denticle belt

denticle row 3 & abdominal 4 ventral denticle belt

denticle row 3 & abdominal 5 ventral denticle belt

denticle row 3 & abdominal 6 ventral denticle belt

denticle row 3 & abdominal 7 ventral denticle belt

denticle row 3 & abdominal 8 ventral denticle belt

denticle row 4 & abdominal 2 ventral denticle belt

denticle row 4 & abdominal 3 ventral denticle belt

denticle row 4 & abdominal 4 ventral denticle belt

denticle row 4 & abdominal 5 ventral denticle belt

denticle row 4 & abdominal 6 ventral denticle belt

denticle row 4 & abdominal 7 ventral denticle belt

denticle row 4 & abdominal 8 ventral denticle belt

leg & joint

tarsal segment 1 & joint

tarsal segment 2 & joint

tarsal segment 3 & joint

tarsal segment 4 & joint

tarsal segment 5 & joint

Detailed Description
Statement
Reference

Mutant male first instar larvae raised at 25[o]C show a reduction in the number of hub cells in the gonad compared to controls.

SerRX106/+ markedly enhances the loss of eye tissue caused by expression of mir-8SC1 under the control of Scer\GAL4ey.PH.

Homozygous intestinal stem cell (ISC) clones in the adult midgut show normal development.

The second mitotic wave occurs normally in clones of SerRX106 mutant cells in a Minute/+ background in the eye disc.

SerRX106 mutants display no lateral inhibition defects in sensory organ precursors in third instar nota.

In SerRX106 homozygous embryos the distal ends of the salivary gland ducts are enlarged/splayed in the region where they contact the secretory cells.

Mutant embryos form normal looking hindgut boundary cells.

Pupal lethal when heterozygous with the MBT chromosome.

SerRX106/Df(3R)D605 animals do not survive but a few mutant flies are formed inside the pupal cases. These flies have leg deformities, lacking the joints between all segments, although sometimes a remnant of a constriction can be seen. No other leg area is affected and the segment boundaries of the leg are still present as shown by the apical bristles in the tarsi and tibia.

Embryos do not show any abnormality in the overall pattern of the tracheal system.

SerRX106/SerCS94 animals show loss of wing disc tissue.

Homozygous DlRevF10 SerRX106 double mutant clones in the leg result in a failure to form joints. In most cases, the failure to form joints is an autonomous property of the mutant cells in the clone.

Approximately half of homozygous larvae show complete fusion of denticle rows 3 and 4 in abdominal segments A2 to A8. The denticles in the fused row have no regular polarity and about half the larvae develop small denticles in this row. Ubiquitous expression of SerScer\UAS.cGa under the control of Scer\GAL4arm.PS in a SerRX106/Df(3R)Bd background results in severe morphological defects; the mouth hooks develop additional sclerotic material at the middle and base and about a quarter of the embryos show duplication of the mouth hook tips. Extra sclerotic material also develops in the dorsal pouch. The phenotype varies from an extended and fragmented dorsal bridge to extreme sclerotisation of the dorsal pouch and shortening of the lateralgraten. Excessive sclerotisation is seen in the proventriculus and gut. Homozygous and wild-type embryos show comparable patterns of BrdU incorporation during the final round of ventral epidermal cell division.

SerCS94/SerRX106 flies develop a very small wing and hinge.

SerCS94/SerRX106 flies have a small marginless wing blade.

Neural differentiation does not occur in DlRevF10 SerRX106 double mutant clones in the eye disc, except near the clone margins. Where neural differentiation occurs near the clone margins, excessive numbers of R8 cells are seen. This phenotype resembles that seen for clones homozygous for Dl- alone.

Homozygous clones in the adult scutum have normal bristle structures. Homozygous clones induced in the sensory organ lineage have a similar phenotype to homozygous SerRX82 clones induced in the sensory organ lineage.

Loss of Ser function has no discernible effect on R8 differentiation in the eye disc (clonal analysis).

Homozygous clones abutting the wing margin in the dorsal wing compartment or induced before dorso-ventral lineage segregation cause extensive wing scalloping.

Df(3R)D605/SerRX106 flies have wings reduced to stumps that have no margin.

Anterior spiracles do not develop knob-like structure typical of first and second larval instar, nor the retractable fingerlike structures characteristic of third instar larvae. The tracheal trunk terminates without opening to the exterior anteriorly, but the posterior spiracles look normal. Mouth hooks always exhibit features characteristic of first instar larvae. Some imaginal discs are smaller than wild type, particularly the dorsal mesothoracic discs. The size of the humeral disc appears normal. Pharate adult escapers are lacking wings and halteres, genital apparatus and anal plates are small or missing, tarsal segments are fused and eyes are rough and reduced. Clones induced in adults are normal in head, thorax legs and abdomen, but produce nicking and deletions in the wing.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference

Ser[+]/SerRX106 is an enhancer of visible phenotype of Scer\GAL4ey.PH, mir-8SC1

Ser[+]/SerRX106 is an enhancer of visible phenotype of fjN7

Suppressor of
Statement
Reference

Ser[+]/SerRX106 is a suppressor | partially of visible | heat sensitive phenotype of Dcr-2UAS.cDa, EogtGD5084, Scer\GAL4en.PU

Ser[+]/SerRX106 is a suppressor | partially of visible phenotype of mir-8Δ2/Df(2R)mir-8Δ3

Ser[+]/SerRX106 is a suppressor of abnormal size phenotype of mir-8Δ2/Df(2R)mir-8Δ3

Other
Phenotype Manifest In
Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

Ser[+]/SerRX106 is a non-enhancer of eye phenotype of Scer\GAL4ey.PH, fngUAS.cKa

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

The wing blistering phenotype seen in the posterior compartment of wings in flies expressing EogtGD5084 under the control of Scer\GAL4en.PU in the presence of Dcr-2Scer\UAS.cDa is dominantly partially suppressed if the flies are also heterozygous for SerRX106.

DlRevF10, SerRX106 double mutant clones in the adult thorax exhibit external sensory cell loss and an excess of neurons.

A DlRevF10 SerRX106 double mutant background suppresses the extra socket cell phenotype seen in AP-47SHE-11 thorax clones, instead producing the external sensory cell loss and excess neurons seen in DlRevF10 SerRX106 double mutants.

Wing disc clones mutant for DlRevF10 and SerRX106 give rise to clustered supernumerary sensory organ precursors (SOP), as all cells within the proneural field adopt the SOP fate. These are often spaced apart from each other, suggesting that a low level of lateral inhibition is still taking place.

Expression of DlΔICD2.Scer\UAS.T:SV5\V5,T:Zzzz\His6 under the control of the ubiquitous driver Scer\GAL4mat.αTub67C.T:Hsim\VP16 restores N signalling in DlRevF10 SerRX106 mutant clones, leading to individualised sensory organ precursors. These are often spaced apart from each other, suggesting that a low level of lateral inhibition is still taking place.

Expression of DlΔICD1.Scer\UAS.T:SV5\V5,T:Zzzz\His6 or DlΔICD1.ΔICD2.Scer\UAS.T:SV5\V5,T:Zzzz\His6 under the control of the ubiquitous driver Scer\GAL4mat.αTub67C.T:Hsim\VP16 fails to restore lateral inhibition by N signalling in DlRevF10 SerRX106 mutant clones. These are often spaced apart from each other, suggesting that a low level of lateral inhibition is still taking place.

Expression of DlΔC.Scer\UAS.T:SV5\V5,T:Zzzz\His6 or DlK742R.Scer\UAS.T:SV5\V5,T:Zzzz\His6 under the control of the ubiquitous driver Scer\GAL4mat.αTub67C.T:Hsim\VP16 fails to restore lateral inhibition N signalling in DlRevF10 SerRX106 mutant clones.

Expression of DlScer\UAS.T:Hsap\LDLR-int,T:Hsap\MYC under the control of the ubiquitous driver Scer\GAL4Scer\FRT.Rnor\CD2.Act5C does not rescue N-mediated lateral inhibition in DlRevF10 SerRX106 mutant clones, as a large number of adjacent sensory organ precursors are reproducibly detected.

SerRX106/+ fully rescues the defects in wing size and partially suppresses the extra wing vein phenotype caused by mir-8Δ2/Df(2R)mir-8Δ3.

DlRevF10 SerRX106 third instar nota clones exhibit at least eight sensory organ precursors (SOPs) in approximately 70.5% of SOP positions scored. Approximately 21.5% of SOP positions display between four and eight ectopic SOPs, while approximately 6% exhibit between one and four SOPs, with only 2% exhibiting one SOP, as in wild-type. Addition of the DlScer\UAS.cLa transgene, under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16 partially rescues the ectopic SOP phenotype, with approximately 8.5% of SOP positions exhibiting between four and eight SOPs. Addition of the SerScer\UAS.cGa transgene, under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16, partially rescues the ectopic SOP phenotype, with approximately 26% of SOP positions exhibiting between one and four SOPs. neur1 SerRX106 third instar nota clones exhibit at least eight sensory organ precursors (SOPs) in approximately 33.5% of SOP positions scored. Approximately 47% of SOP positions display between four and eight ectopic SOPs, while approximately 19.5% exhibit between one and four SOPs. No SOP positions appeared wild-type. Addition of the SerScer\UAS.cGa transgene, to DlRevF10 SerRX106 double mutant third instar nota clones, under the control of Scer\GAL4mat.αTub67C.T:Hsim\VP16, partially rescues the ectopic SOP phenotype, with approximately 26% of SOP positions exhibiting between one and four SOPs.

The small eye phenotype of flies in which fngScer\UAS.cKa is expressed under the control of Scer\GAL4ey.PH is not enhanced in SerRX106 heterozygotes.

The loss of wing disc tissue seen in SerRX106/SerCS94 animals is rescued by DlScer\UAS.cHa expressed under the control of Scer\GAL4dpp.blk1.

DlRevF10,SerRX106 double mutant somatic clones in wing discs fail to respect the dorsal ventral boundary.

Enhances the Dfd13/Dfd3 phenotype; reduces the survival of Dfd13/Dfd3 hypomorphs. All of the denticles in rho6 SerRX106 double mutant embryos are similar to each other and resemble a composite of type 5 and 2 denticles. The denticles are disorganised and separate rows are not distinguishable.

Scer\GAL4dpp.blk1-mediated expression of vgScer\UAS.cKa substantially rescues the wing blade.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
Comments
Comments

See Thomas et al., 1991, Development 111:749--761 .

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (7)
References (55)