Open Close
General Information
Symbol
Dmel\spi1
Species
D. melanogaster
Name
FlyBase ID
FBal0016005
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
spiA14, spiIIA14, spiIIA, spi2A14, spitzIIA
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
point mutation
Nucleotide change:
G19568646A
Reported nucleotide change:
G8670A
Amino acid change:
G118R | spi-PA; G118R | spi-PB; G118R | spi-PE; G118R | spi-PF; G118R | spi-PG
Reported amino acid change:
G118R
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Amino acid replacement: G118R.
Missense mutation in conserved part of EGF-like domain.
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 )
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
lamina & neuron
sensory neuron & axon & embryo
Detailed Description
Statement
Reference
spi1 mutant embryos show cardioblast (CB) patterning defects and significantly fewer cardioblasts, specifically generic cardioblasts leading to lower generic CBs:ostial CBs ratio than the typical 4:2 ratio. These embryos also exhibit a significant decrease in the number of odd pericardial cells, although even pericardial cells are unaffected, as compared to controls.
The concentration of circulating hemocytes in spi1 heterozygous third instar larvae is comparable to that in wild-type controls.
spi1/+ heterozygotes display normal patterning and cell numbers in pupal retina.
spi1 mutant embryos exhibit defects in ventral patterning. The denticle belts are narrow and some are fused.
Small clones of spi1 glial cells recovered using MARCM show no effect in the underlying larval neuroepithelium or in the final optic lobe size.
Mutant embryos show a decrease in the number of dorsolateral and lateral adult muscle precursor cells compared to wild type.
Flies heterozygous for spi1 have normal cardiac function.
The proliferation of spi1 mutant clones of adult midgut progenitor cells is normal.
Eggs derived from egg chambers containing complete homozygous follicle cell clones appear normal and have two dorsal appendages.
Clones in third instar eye discs do not show defects in R8 spacing or cell clustering behind the furrow. Only slightly elevated levels of cell death are observed.
spi1 Minute clones in the eye disc do not affect the formation of rosettes and arcs of cells in the morphogenetic furrow.
In spi1 embryos, apoptosis is induced throughout the cells of the posterior compartment.
Homozygous embryos have a reduced number of midline glia per ventral nerve cord segment compared to wild type.
94% of cuticles from spi1 homozygous embryos show fusion of at least one pair of denticle belts, with the majority having between 1 and 3 fusions. During stages 10-14, embryos of this genotype have increased levels of apoptosis in epidermis around the ventral midline.
No increase is seen in cardioblast numbers in the developing embryo.
Metameric furrow form and are maintained normally in spi1 homozygous embryos.
In spi1 mutant embryos, sensory axons project abnormally across segment boundaries and glial morphology is abnormal. Additionally, the anterior and posterior sensory fascicles are spaced further apart at the CNS-PNS transition zone compared to wild type.
The number of midline glial cells in spi1 homozygous stage 17 embryos is greatly reduced compared to wild-type.
Homozygous clones in the adult abdomen do not show any consistent alterations of normal polarity.
Homozygous somatic clones in the legs and wings have bractless mechanosensory bristles.
Border cells still migrate dorsally when all dorsal follicle cells are mutant for spi1 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. Oenocyte precursor whorls are missing in stage 11 embryos.
The number of neurons in the lch5 organ is reduced from five to three in mutant embryos. Late stage embryos show a loss of oenocytes.
2.4 +/- 0.4 midline glia (MG) are seen per segment in stage 12/0 mutant embryos (wild-type embryos have 5.6 +/- 0.2 MG cells per segment at this stage). At stage 17 mutant embryos have 1.9 +/- 0.8 MG per segment compared to the wild type 3.0 +/- 0.1 MG per segment. The number of midline cells in the dorsal nerve cord is reduced in mutant stage 16 embryos, while the ventral cell number and position are unaffected. Thickening and fusion of the commissures and thinning of the longitudinal tracts is seen.
In spi1 somatic clones in the eye disc, the amount of apoptosis seen is slightly above that seen in wild-type.
The Bolwig's organ is smaller than normal in mutant embryos. The posterior lip of the optic lobe is reduced in size.
Homozygous spi1 clones in the wing have no effect on vein patterning.
spi1 embryos have the normal number of eve-expressing pericardial cells (EPCs) but no DA1 muscles. spi1; zfh12 embryos have no EPCs and no DA1 muscles. spi1 embryos in which numbfl.Scer\UAS.T:Hsap\MYC is expressed under the control of Scer\GAL4how-24B and Scer\GAL4twi.PG lack the EPCs and DA1 muscles.
Homozygous embryos lack approximately half of the normal myofibres; gaps are present in the set of ventral longitudinal muscles and only one of the normal 3 ventral oblique muscles is present, although all lateral transverse muscles develop normally. The precursor of muscle DA1 is missing. Muscles DO1, LT2 and LT4, and the eve-expressing pericardial cell precursors form normally. The P15 muscle precursor cell does not form. Apoptosis within the mesoderm is significantly higher than in wild-type embryos, and myoblasts engulfed by macrophages are seen.
Embryos show loss of optic lobe and Bolwig's organ and reduction of dorsomedial and ventromedial brain, the stomatogastric nervous system, the hypocerebral ganglion and the recurrent nerve.
spi1/astK6 double heterozygotes do not have a visible phenotype.
Germline clones fail to rescue the female sterile phenotype of Fs(2)Ugr.
Early CNS development is essentially normal in mutant embryos.
spiSCP2/spi1 hypomorphic females lay eggs that show a significant loss of the most dorsal tissue. Germline clones reveal no requirement for spi in patterning the egg, or in the viability or patterning of the embryo.
In homozygous larvae the most ventral denticle belts are absent and denticle rows are fused between segments. In spi1; CrebAwR23 mutants the denticle bands are narrower with some fusion of denticles between segments.
Either no dorsal medial cells or reduced numbers of cells form.
spi1/spiVA17 embryos exhibit deletion of ventral denticles so the width of the belt is reduced. Wing, leg, haltere and eye/antenna spi1/spiVA17 mutant discs can be in vivo cultured.
In mutant eye clones the initial single neuron stage ommatidia appear normal, as do their spacing. However no further progression occurs, and the clusters appear to be arrested at the one neuron stage. The wave of DNA synthesis immediately following the furrow is unaffected in spi mutant clones. The early development of the preclusters is normal up until the 5-cell stage. Development proceeds normally anterior to and in the furrow (up to the specification and early differentiation of the founding R8 photoreceptor cells) but the specification of R2 and R5, and all subsequent steps, fail. Homozygous spi mutant clones are apparently equal in size to their homozygous wild-type twin-spots.
No effect on the faf eye phenotype.
Mitotic clones have reduced numbers of photoreceptors and loss of whole ommatidia.
Retinal clones induced during first larval instar show defects in the formation of photoreceptor cells R8, R2, R5, R3 and R4.
Nondefective in gonad assembly.
Malpighian tubules of homozygous embryos are short and each contains an average of only 39 cells.
All or nearly all of the ventral epidermal cells are absent in mutant embryos.
Salivary placodes are expanded towards the ventral midline.
Epidermal defects and fusion of the anterior and posterior commissures. In the PNS some sensory organs are missing, there is a ventral-dorsal gradient of severity. Several muscle fibres are always missing in the dorsolateral region and there are variable abnormalities in the number, shape and attachment sites of the eight ventral oblique muscle fibres.
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 are present but fail to migrate.
embryonic lethal
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference
spi1/spi[+] is a non-enhancer of visible phenotype of vnL6/vn1
spi1/spi[+] is a non-enhancer of visible phenotype of Scer\GAL4Tub.PU, cswN308D.UASp
spi1 is a non-enhancer of visible phenotype of CanBGMR.PS, Pp2B-14Dact.GMR
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
spi1/spi[+] is a non-suppressor of neuroanatomy defective | third instar larval stage phenotype of Nf1E2
spi1/spi[+] is a non-suppressor of visible phenotype of Scer\GAL4Tub.PU, cswN308D.UASp
spi1 is a non-suppressor of visible phenotype of CanBGMR.PS, Pp2B-14Dact.GMR
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
spi1 has denticle belt phenotype, enhanceable by vnL6
spi1, vnL6 has denticle belt phenotype, enhanceable by Krn27
Krn27, spi1 has denticle belt phenotype, enhanceable by vnL6
spi1 has denticle belt phenotype, enhanceable by Krn27
Egfrf1, spi1 has somatic muscle | embryonic stage phenotype, enhanceable by S[+]/SIIN
spi1 has phenotype, enhanceable by vnL6
spi1 has phenotype, enhanceable by vnddd-4
NOT Enhanced by
Statement
Reference
Krn27, spi1, vnL6 has denticle belt phenotype, non-enhanceable by grkHF
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference
spi1/spi[+] is an enhancer of wing blade phenotype of sl2
spi1 is an enhancer of ommatidium phenotype of S48-5
spi1 is an enhancer of interface glial cell phenotype of vnγ4
spi1 is an enhancer of somatic muscle | embryonic stage phenotype of Egfrf1, SIIN
spi1 is an enhancer of egg phenotype of Ras85Dix12a
spi1 is an enhancer of phenotype of EgfrE1
NOT Enhancer of
Statement
Reference
spi1/spi[+] is a non-enhancer of wing vein L3 phenotype of vnL6/vn1
spi1/spi[+] is a non-enhancer of NMJ bouton | supernumerary | third instar larval stage phenotype of Nf1E2
spi1/spi[+] is a non-enhancer of wing vein | ectopic phenotype of sl2
spi1 is a non-enhancer of border follicle cell phenotype of Pvf1EP1624
spi1/spi[+] is a non-enhancer of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp
spi1 is a non-enhancer of eye phenotype of CanBGMR.PS, Pp2B-14Dact.GMR
spi1 is a non-enhancer of wing vein phenotype of vn1
Suppressor of
Statement
Reference
spi1/spi[+] is a suppressor of hemocyte | supernumerary | third instar larval stage phenotype of Graf1
spi1 is a suppressor | partially of retina | pupal stage phenotype of Vav2
spi1 is a suppressor | partially of retina | pupal stage phenotype of Vav3
spi1 is a suppressor of eye phenotype of RetMEN2B.GMR
spi1 is a suppressor of eye phenotype of RetMEN2A.GMR
spi1/spi[+] is a suppressor of ommatidium phenotype of jingUAS.cSa
spi1 is a suppressor of phenotype of arm3
spi1 is a suppressor of egg phenotype of rhohs.PSt
spi1 is a suppressor of phenotype of rhohs.sev
spi1 is a suppressor of phenotype of EgfrE3
spi1 is a suppressor of phenotype of S218
NOT Suppressor of
Statement
Reference
spi1/spi[+] is a non-suppressor of NMJ bouton | supernumerary | third instar larval stage phenotype of Nf1E2
spi1/spi[+] is a non-suppressor of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp
spi1 is a non-suppressor of eye phenotype of Scer\GAL4ey.PH, brmK804R.UAS.Tag:HA
spi1 is a non-suppressor of eye phenotype of CanBGMR.PS, Pp2B-14Dact.GMR
spi1 is a non-suppressor of phenotype of Src42ASu(Raf)1-1
Other
Additional Comments
Genetic Interactions
Statement
Reference
The increased concentration of circulating hemocytes characteristic for Graf1/Y mutant third instar larvae is suppressible by combination with a single copy of spi1.
The supernumerary cone cells in pupal retina observed in either Vav2 or Vav3 mutants is almost completely suppressed by combination with spi1 in heterozygous state but the increased number of primary pigment cells remains unchanged.
vnL6 enhances the ventral patterning defects seen in spi1 mutant embryos. The double mutants have a reduced number of denticle belts compared to controls, fusion of the denticle belts and an anterior hole. The phenotype is further exacerbated by Krn27, with embryos having no denticle belts and a large anterior hole. A zygotic grkHF mutation has no additional effect. Krn27 enhances the ventral patterning defects seen in spi1 mutant embryos. The double mutants have a reduced number of denticle belts compared to controls, fusion of the denticle belts and an anterior hole. The phenotype is further exacerbated by vnL6, with embryos having no denticle belts and a large anterior hole. A zygotic grkHF mutation has no additional effect. Krn27/Krn9 enhances the wing vein phenotypes seen in vnL6/vn1 mutants. A greater proportion of flies show longitudinal vein 3 loss than in vnL6/vn1 alone. The phenotype is further enhanced by one copy of spi1. One copy of spi1 does not enhance the vein phenotypes seen in vnL6/vn1 mutant wings.
The increase in mean number of boutons per neuromuscular junction which is seen in Nf1E2 third instar larvae is not suppressed by spi1/+.
The extra wing vein phenotype caused by expression of CG4096KK108644 under the control of Scer\GAL4Act5C.PU is not suppressed if the flies also carry spi1. The extra wing vein phenotype caused by expression of CG4096KK108644 under the control of Scer\GAL4Act5C.PU is not suppressed if the flies also simultaneously carry vnL6 and spi1. The extra wing vein phenotype caused by expression of CG4096KK108644 under the control of Scer\GAL4Act5C.PU is significantly suppressed if the also simultaneously carry both spi1 and Krn27. The suppression is more pronounced if the flies simultaneously carry spi1, Krn27 and vnL6.
Heterozygosity for spi1 in a Df(3L)Krn-27-7-B mutant background (spi1/+; Df(3L)Krn-27-7-B/Df(3L)Krn-27-7-B) significantly reduces Pseudomonas entomophila-induced intestinal stem cell proliferation.
One copy of spi1 enhances the reduction in wing blade area seen in homozygous sl2 males. One copy of spi1 does not enhance the ectopic wing vein phenotype seen in sl2 homozygotes. One copy of spi1 partially suppresses the percentage of sl2 mutant ommatidia that contain extra R7 photoreceptors. The number of R7 cells per ommatidium is also reduced.
Germaria with germ line double mutant for grkunspecified and spi1 do not exhibit ectopic spectrosome containing cells. Germaria with germ line triple mutant for Df(3L)Krn-27-7-B, grkunspecified and spi1 exhibit ectopic spectrosome containing cells.
The proliferation of spi1 mutant clones of adult midgut progenitor cells generated in a Df(3L)Krn-27-7-B homozygous mutant background is normal.
The presence of a spi1 background causes minor suppression of ectopic wing vein formation found in cswY279C.Scer\UAS (Scer\GAL4tub) mutants.
spi1 clones made in the Df(3L)Krn260 background in third instar eye discs show irregular spacing of R8 cells, cell clustering defects behind the furrow, and contain large numbers of cells undergoing apoptosis.
Pvf1EP1624; spi1 double mutant egg chambers show no enhancement of the border cell migration defects seen in Pvf1EP1624 single mutants. Pvf1EP1624; spi1; Df(3L)Krn-27-7-B triple mutants are poorly viable or sterile. The egg chambers of Pvf1EP1624; spi1; grkHF females do not develop normally.
Expression of CycEScer\UAS.cLa, under the control of Scer\GAL4en-e16E, in spi1 embryos increases cell death in the posterior compartment, relative to expression of CycEScer\UAS.cLa in a wild-type background.
The increase in the number of midline glia per ventral nerve cord segment seen in embryos expressing jingScer\UAS.cSa under the control of Scer\GAL4sli.PS is not suppressed by spi1, but expression of jingScer\UAS.cSa under the control of Scer\GAL4sli.PS in a homozygous spi1 background does not induce extra midline glia and the number of midline glia per ventral nerve cord segment in these double mutant embryos is reduced compared to wild type and is similar to that seen in homozygous spi1 single mutants. The rough eye phenotype caused by expression of jingScer\UAS.cSa under the control of Scer\GAL4GMR.PF is dominantly suppressed by spi1. jing01094/spi1 double heterozygous embryos have a reduced number of midline glia per ventral nerve cord segment compared to wild type. jing3/spi1 double heterozygous embryos have an increased number of apoptotic cells in the CNS midline at stage 12 compared to wild type (where cell death is uncommon at this stage). jing3/spi1 double heterozygous embryos have breaks in the dorsal trunk of the tracheal system at stage 15.
S48-5/spi1 mutants show 40.04%+-3.7 misrotated ommatidia compared to 9.55%+-1.43 seen in S48-5 mutants alone.
The loss of midline glial (MG) cells in spi1 homozygous embryos is suppressed by WrvX1/WrvX1. Approximately twice as many MG cells survive as in wild-type (average of 5.7 per segment n=133, compared to average = 2.8 for wild-type).
Weakly enhances the eye phenotype produced by activated arm constructs. (either armS44Y.GMR or armS56F.GMR).
The decrease in interface glial cell numbers and increase in interface glial cell apoptosis seen in vnγ4/Df(3L)γ3 are both enhanced by spi1/spi1.
salm3 spi1 double mutant embryos have an average of 3 +/- 0.08 neurons per lch5 organ, similar to spi1 single mutant embryos. The embryos show misplacement of the lch5 organ along the dorsoventral axis comparable to the phenotype seen in salm single mutants.
spi1 ; vnunspecified double homozygotes have one dorsal midline cell per segment and a reduction in the number of ventral neurons. The effect on the dorsal midline cells appears to be additive, while the effect on the number of ventral neurons suggests a genetic interaction between spi and vn. Most spi1 ; vnunspecified double homozygotes show complete fusion of the commissures and complete loss of the longitudinal tracts. Some embryos lack both longitudinal and commissural connectives, with most axons remaining within one hemi-segment. vnunspecified homozygotes that are also heterozygous for spi1 have a single fused commissure and variably reduced longitudinal connectives.
In vn1 homozygotes, there is no exacerbation of the loss of vein phenotype within homozygous spi1 clones in the wing.
The ubiquitous expression of rhohs.PSt under heatshock leads to a partial suppression of the spi1 loss of midline glial cell phenotype. No significant suppression of the axon tract phenotype is seen, however longitudinal tracts are thinner in these embryos. (this effect is not seen when rhohs.PSt is added to wild-type embryos). Commissure separation in rhohs.PSt,spi1 is not improved.
Does not suppress the ability of Src42ASu(phl)1-1 to suppress the lethality of phl1/Y flies.
The mild Egfrf1 muscle phenotype is not affected by one copy of spi1 alone, but spi1 shows additional enhancement of the muscle phenotype in combination with SIIN.
Reduction in dose of spi rescues the rhohs.sev eye to a near wild-type phenotype; regular array of ommatidia, regular arrangement of photoreceptors and unbroken lattice of pigment cells. Rescue is not always complete. Reduction of the dose of spi causes some suppression of the EgfrE3 rough eye phenotype; more ommatidia and increase in the size of the eye.
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Fails to complement
Partially rescued by
Not rescued by
Comments
Unlike spiScer\UAS.cSa; Scer\GAL4da.G32, spiCS.m.Scer\UAS; Scer\GAL4da.G32 completely fails to rescue lethality due to spi1/spiSC1.
Animals heterozygous for spiSCP2 and spi1 which have been rescued by spiScer\UAS.cSa with Scer\GAL4hs.PB to the third instar stage show relatively normal ommatidial development at the posterior of the eye imaginal disc. More anterior columns of ommatidia have reduced photoreceptors. In the lamina, retinal projections appeared normal but LPCs show no neuronal differentiation. This phenotype is rescued by the introduction of Scer\GAL4GMR.PF or in clones induced to produce Scer\GAL4αTub84B.PP.
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments
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.
No interaction with P{sev-svp1} or P{sev-svp2} exists.
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (12)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (97)