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General Information
Symbol
Dmel\spir1
Species
D. melanogaster
Name
FlyBase ID
FBal0016011
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
spirRP, spirRP48, spireRP
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

G20334710T

Amino acid change:

E292term | spir-PA; E292term | spir-PB; E292term | spir-PD; E292term | spir-PE; E292term | spir-PF; E292term | spir-PG; E292term | spir-PH; E292term | spir-PI; E292term | spir-PJ

Reported amino acid change:

E292term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Amino acid replacement: E292term.

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
Detailed Description
Statement
Reference

spir1/Df(2L)Exel6046 females are sterile. Their eggs do not hatch. Their oocytes lack actin mash at any stage and they exhibit premature onset of fast cytoplasmic streaming.

Expression of Scer\GAL4nos.UTR.T:Hsim\VP16>spirRD.Scer\UAS.P\T.T:Avic\GFP in spir1/Df(2L)Exel6046 females results in oocytes with an actin mesh and fast streaming is prevented. When fertility is measured, only 12% of the eggs laid by the mutant flies hatch.

spir1/Df(2L)Exel6046 females expressing Scer\GAL4nos.UTR.T:Hsim\VP16>spirScer\UAS.P\T.RB.T:Avic\GFP are mostly fertile: 59% of the eggs hatch.

spir1/Df(2L)Exel6046 females expressing Scer\GAL4nos.UTR.T:Hsim\VP16>spirScer\UAS.P\T.RB are mostly fertile: 48% of the eggs hatch.

spir1/Df(2L)Exel6046 females expressing Scer\GAL4nos.UTR.T:Hsim\VP16>spirY232K.Scer\UAS.P\T.RB.T:Avic\GFP are sterile. The mutant oocytes have no detectable actin mesh during mid-oogenesis and consistently exhibit premature streaming. At later stages of oogenesis, no mesh is visible and fast streaming is observed at stage 11.

Mutant oocytes show premature cytoplasmic streaming at stage 9. In addition, the microtubules are aligned in arrays along the oocyte cortex, instead of the wild-type anterior-to-posterior gradient.

Mutant stage 9 oocytes do not contain the actin mesh (a uniform network of actin filaments present throughout the cytoplasm) that is seen in wild-type oocytes at this stage. Any remaining cytoplasmic F-actin in the mutant oocytes forms small dots.

25-30% of oocytes in spir1 mutants show severe defects in karyosome morphology and abnormal G-actin accumulation.

The oocyte nucleus fails to localise properly to its normal anterodorsal position in the egg chambers of homozygous females.

Dorsalised egg chambers.

Prevents the posterior accumulation of G-iα65A protein.

hts RNA localization unaltered in embryos derived from spir mutant mothers.

spir1;6xP{osk+108} embryos exhibit a class of embryos with abdominal deletions typical of posterior group mutations.

Strong abdominal defects.

Does not interact with RpII140wimp maternal effect.

Variable expansion (dorsalization) of dorsal appendages, at expense f main body shell. Absence of polar granules, pole cells and abdominal segments in embryos.

Localization of vas protein to pole cells and polar granules abolished.

Homozygous spir1 embryos derived from homozygous females have no polar granules, fail to form pole cells, have deletions of abdominal structures and defects associated with dorsal/ventral pattern formation. Posterior localization of vas and CycB transcripts is completely abolished.

Homozygous mothers produce dorsalized egg shells and embryos. The first sign of dorsalization in embryos can be seen during gastrulation, when the ventral furrow is reduced or absent. Dorsalization in the egg chamber is evident in the shape of the follicle cells. While the number of follicle cells around the main body of the egg shell is reduced, dorsal appendages are expanded, often fused dorsally and/or extended ventrally. The embryos lack polar granules and pole cells, and show cellularization defects. Embryos show abdominal segmentation defects similar to those produced by mutations in the grandchildless-knirps or posterior class of maternal effect loci.

maternal-effect lethal homozygous females lay eggs which sometimes (5-10%) have a "peak" (spire) of dorsal appendage material sitting over the anterior end of the egg, instead of two distinct dorsal appendages. Such eggs are similar to eggs formed by the female-sterile mutation fs(1)K10, but the extent of dorsal appendage material on spir eggs is much more variable than that of fs(1)K10 eggs. Mutant females produce embryos lacking polar granules, pole cells and normal abdominal segmentation. In combination with BicD, however, abdominal segmentation does develop in the anterior half of the embryo; improper localization of abdominal determinants also indicated by the lack of posterior localization of vasa protein. Cellularization of the blastoderm irregularly defective with nuclei of different sizes and densities. Resemble embryos formed by other grandchildless-knirps-like mutations, such as vasa or tudor, but in addition, some of the embryos from spire females appear also to be dorsalized.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Suppressed by
Enhancer of
Statement
Reference

spir[+]/spir1 is an enhancer of ellipsoid body phenotype of ccbks127

spir[+]/spir1 is an enhancer of ellipsoid body phenotype of ccbks145

NOT Enhancer of
Statement
Reference

spir[+]/spir1 is a non-enhancer of phenotype of ctL188

spir[+]/spir1 is a non-enhancer of phenotype of ctC145

spir1 is a non-enhancer of phenotype of ctC145

Suppressor of
Statement
Reference

spir[+]/spir1 is a suppressor | partially of embryonic head phenotype of miraαTub67C.mGFP6

Additional Comments
Genetic Interactions
Statement
Reference

The bicaudal phenotype of embryos derived from miraαTub67C.T:Avic\GFP-m6/+ females is suppressed if the females are also heterozygous for spir1.

Expression of capuΔN.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 suppresses the premature cytoplasmic streaming seen in spir1 oocytes until the end of stage 9. The microtubules show a nearly wild-type organisation at stage 9 in the rescued oocytes, but this rescue is temporary as at stage 10A most of the oocytes show cortical arrays of microtubules.

The loss of the actin mesh in the cytoplasm of stage 9 spir1 oocytes is rescued by expression of capuΔN.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16, although the mesh appears less dense than in wild type. Ectopic actin mesh-like structures are also induced in the nurse cells in these animals.

Overexpression of Cf2s.hs can reduce the dorsalising effects, some eggs display two distinct dorsal appendages. Overexpression during oogenesis similarly rescues the maternal dorsalising effect so some embryos have restored ventral denticles.

Injection of nosN5 RNA into homozygous embryos completely rescues the abdominal phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments

Expression of Scer\GAL4nos.UTR.T:Hsim\VP16>spirRD.Scer\UAS.P\T.T:Avic\GFP in spir1/Df(2L)Exel6046 females results in oocytes with an actin mesh and fast streaming is prevented. When fertility is measured, only 12% of the eggs laid by the mutant flies hatch.

spir1/Df(2L)Exel6046 females expressing Scer\GAL4nos.UTR.T:Hsim\VP16>spirScer\UAS.P\T.RB.T:Avic\GFP are mostly fertile: 59% of the eggs hatch.

spir1/Df(2L)Exel6046 females expressing Scer\GAL4nos.UTR.T:Hsim\VP16>spirScer\UAS.P\T.RB are mostly fertile: 48% of the eggs hatch.

spir1/Df(2L)Exel6046 females expressing Scer\GAL4nos.UTR.T:Hsim\VP16>spirY232K.Scer\UAS.P\T.RB.T:Avic\GFP are sterile. The mutant oocytes have no detectable actin mesh during mid-oogenesis and consistently exhibit premature streaming.

Expression of spirRC.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 does not rescue the premature cytoplasmic streaming seen in stage 9 spir1/Df(2L)Exel6046 oocytes.

Expression of spirRD.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16 rescues the premature cytoplasmic streaming seen in stage 9 spir1/Df(2L)Exel6046 oocytes. The fast cytoplasmic streaming that is normally seen during stages 11-13 is prevented in these oocytes.

The loss of the actin mesh in the cytoplasm of stage 9 spir1/spir2F oocytes is rescued by expression of spirRD.Scer\UAS.P\T.T:Avic\GFP under the control of Scer\GAL4nos.UTR.T:Hsim\VP16. Ectopic actin mesh-like structures are also induced in the nurse cells in these animals.

Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Transcripts from oskolc1 behave as those of the endogenous osk gene.

Mutation does not affect posterior follicle cell determination.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (8)
References (45)