|Feature type||allele||Associated gene||Dmel\spi|
|Also Known As||spiA14, spiIIA14, spiIIA, spi2A14, spitzIIA|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
lamina & neuron
sensory neuron & axon & embryo
Mutant embryos show a decrease in the number of dorsolateral and lateral adult muscle precursor cells compared to wild type.
The proliferation of spi 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.
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 somatic clones in the legs and wings have bractless mechanosensory bristles.
Homozygous clones in the adult abdomen do not show any consistent alterations of normal polarity.
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.
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.
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.
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.
|NOT Enhancer of|
spi1/spi[+] is a suppressor of visible phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, jingScer\UAS.cSa
|NOT Suppressor of|
|Phenotype Manifest In|
|NOT suppressed by|
spi1 is an enhancer of embryonic segment | posterior compartment phenotype of CycEScer\UAS.cLa, Scer\GAL4en-e16E
|NOT Enhancer of|
spi1/spi[+] is a non-enhancer of wing vein | ectopic phenotype of Scer\GAL4tub.PU, cswN308D.Scer\UAS.P\T
spi1, vnL6, Krn27 is a suppressor of wing vein | ectopic phenotype of CG4096KK108644, Scer\GAL4Act5C.PU
spi1/Krn27 is a suppressor | partially of wing vein | ectopic phenotype of CG4096KK108644, Scer\GAL4Act5C.PU
spi1/Scer\GAL4tub.PU is a suppressor | partially of wing vein phenotype of Scer\GAL4tub.PU, cswY279C.Scer\UAS.P\T
spi1/spi1 is a suppressor of midline ventral glial cell | ectopic phenotype of Scer\GAL4sli.PS, jingScer\UAS.cSa
|NOT Suppressor of|
spi1/spi[+] is a non-suppressor of midline ventral glial cell | ectopic phenotype of Scer\GAL4sli.PS, jingScer\UAS.cSa
spi1/spi[+] is a non-suppressor of wing vein | ectopic phenotype of Scer\GAL4tub.PU, cswN308D.Scer\UAS.P\T
The extra wing vein phenotype caused by expression of CG4096[KK108644] under the control of Scer\GAL4[Act5C.PU] is not suppressed if the flies also carry spi. The extra wing vein phenotype caused by expression of CG4096[KK108644] under the control of Scer\GAL4[Act5C.PU] is not suppressed if the flies also simultaneously carry vn[L6] and spi. The extra wing vein phenotype caused by expression of CG4096[KK108644] under the control of Scer\GAL4[Act5C.PU] is significantly suppressed if the also simultaneously carry both spi and Krn. The suppression is more pronounced if the flies simultaneously carry spi, Krn and vn[L6].
One copy of spi enhances the reduction in wing blade area seen in homozygous sl males. One copy of spi does not enhance the ectopic wing vein phenotype seen in sl homozygotes. One copy of spi partially suppresses the percentage of sl mutant ommatidia that contain extra R7 photoreceptors. The number of R7 cells per ommatidium is also reduced.
Germaria with germ line double mutant for grk[unspecified] and spi do not exhibit ectopic spectrosome containing cells. Germaria with germ line triple mutant for Df(3L)Krn-27-7-B, grk[unspecified] and spi exhibit ectopic spectrosome containing cells.
The proliferation of spi 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 spi background causes minor suppression of ectopic wing vein formation found in csw[Y279C.Scer\UAS] (Scer\GAL4[tub]) mutants.
spi clones made in the Df(3L)Krn 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.
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.
|Complementation & Rescue Data|
|Partially rescued by|
|Not rescued by|
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.
|Stocks ( 2 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 11 )|
(Urban et al., 2004, Smith et al., 2002, Dequier et al., 2001, Wasserman et al., 2000, Nagaraj et al., 1999, Huang et al., 1998, Chen et al., 1998, Wasserman and Freeman, 1998, Szuts et al., 1998, Huang and Fischer-Vize, 1996, Schweitzer et al., 1995, Freeman, 1994, Begemann et al., 1995, Edgar et al., 1994, Brown et al., 2006, Mao and Freeman, 2009, Jiang and Edgar, 2009)
|Secondary FlyBase IDs|
|References ( 87 )|
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|Recent research papers ( 2 )|