FlyBase Allele Report: Dmel\spi[1]

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.

(Schwarz et al., 2018)

The concentration of circulating hemocytes in spi¹ heterozygous third instar larvae is comparable to that in wild-type controls.

(Kim et al., 2017)

spi¹/+ heterozygotes display normal patterning and cell numbers in pupal retina.

(Martín-Bermudo et al., 2015)

spi¹ mutant embryos exhibit defects in ventral patterning. The denticle belts are narrow and some are fused.

(Austin et al., 2014)

Small clones of spi¹ glial cells recovered using MARCM show no effect in the underlying larval neuroepithelium or in the final optic lobe size.

(Morante et al., 2013)

Mutant embryos show a decrease in the number of dorsolateral and lateral adult muscle precursor cells compared to wild type.

(Figeac et al., 2010)

Flies heterozygous for spi¹ have normal cardiac function.

(Yu et al., 2010)

The proliferation of spi¹ mutant clones of adult midgut progenitor cells is normal.

(Jiang and Edgar, 2009)

Eggs derived from egg chambers containing complete homozygous follicle cell clones appear normal and have two dorsal appendages.

(Lachance et al., 2009)

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.

(Brown et al., 2007)

spi¹ Minute clones in the eye disc do not affect the formation of rosettes and arcs of cells in the morphogenetic furrow.

(Brown et al., 2006)

In spi¹ embryos, apoptosis is induced throughout the cells of the posterior compartment.

(Parker, 2006)

Homozygous embryos have a reduced number of midline glia per ventral nerve cord segment compared to wild type.

(Sonnenfeld et al., 2004)

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.

(Urban et al., 2004)

No increase is seen in cardioblast numbers in the developing embryo.

(Alvarez et al., 2003)

Metameric furrow form and are maintained normally in spi¹ homozygous embryos.

(Larsen et al., 2003)

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.

(Sepp and Auld, 2003)

The number of midline glial cells in spi¹ homozygous stage 17 embryos is greatly reduced compared to wild-type.

(Bergmann et al., 2002)

Homozygous clones in the adult abdomen do not show any consistent alterations of normal polarity.

(Lawrence et al., 2002)

Homozygous somatic clones in the legs and wings have bractless mechanosensory bristles.

(del Alamo et al., 2002)

Border cells still migrate dorsally when all dorsal follicle cells are mutant for spi¹ in females containing homozygous clones.

(Duchek and Rorth, 2001)

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.

(Elstob et al., 2001)

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.

(Rusten et al., 2001)

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.

(Lanoue et al., 2000)

In spi¹ somatic clones in the eye disc, the amount of apoptosis seen is slightly above that seen in wild-type.

(Wasserman et al., 2000)

The Bolwig's organ is smaller than normal in mutant embryos. The posterior lip of the optic lobe is reduced in size.

(Daniel et al., 1999)

Homozygous spi¹ clones in the wing have no effect on vein patterning.

(Guichard et al., 1999)

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 numb^{fl.Scer\UAS.T:Hsap\MYC} is expressed under the control of Scer\GAL4^how-24B and Scer\GAL4^twi.PG lack the EPCs and DA1 muscles.

(Su et al., 1999)

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.

(Buff et al., 1998)

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.

(Dumstrei et al., 1998)

spi¹/ast^K6 double heterozygotes do not have a visible phenotype.

(Kotarski et al., 1998)

Germline clones fail to rescue the female sterile phenotype of Fs(2)Ugr.

(Sapir et al., 1998)

Early CNS development is essentially normal in mutant embryos.

(Skeath, 1998)

spi^SCP2/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.

(Wasserman and Freeman, 1998)

In homozygous larvae the most ventral denticle belts are absent and denticle rows are fused between segments. In spi¹; CrebA^wR23 mutants the denticle bands are narrower with some fusion of denticles between segments.

(Andrew et al., 1997)

Either no dorsal medial cells or reduced numbers of cells form.

(Luer et al., 1997)

spi¹/spi^VA17 embryos exhibit deletion of ventral denticles so the width of the belt is reduced. Wing, leg, haltere and eye/antenna spi¹/spi^VA17 mutant discs can be in vivo cultured.

(Simcox, 1997)

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.

(Tio and Moses, 1997)

No effect on the faf eye phenotype.

(Huang and Fischer-Vize, 1996)

Mitotic clones have reduced numbers of photoreceptors and loss of whole ommatidia.

(Freeman, 1994)

Retinal clones induced during first larval instar show defects in the formation of photoreceptor cells R8, R2, R5, R3 and R4.

(Tio et al., 1994)

Nondefective in gonad assembly.

(Warrior, 1994)

Malpighian tubules of homozygous embryos are short and each contains an average of only 39 cells.

(Baumann and Skaer, 1993)

All or nearly all of the ventral epidermal cells are absent in mutant embryos.

(Kim and Crews, 1993)

Salivary placodes are expanded towards the ventral midline.

(Panzer et al., 1992)

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.

(Rutledge et al., 1992)

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.

(Klambt et al., 1991)

embryonic lethal

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

spi¹ has cell death defective | somatic clone | third instar larval stage phenotype, enhanceable by Df(3L)Krn²⁶⁰

(Brown et al., 2007)

Enhancer of

Statement

Reference

spi¹/spi[+] is an enhancer of size defective | adult stage phenotype of sl²

(Murillo-Maldonado et al., 2011)

spi¹ is an enhancer of increased cell death | embryonic stage phenotype of CycE^UAS.cLa, Scer\GAL4^en-e16E

(Parker, 2006)

spi¹ is an enhancer of cell polarity defective phenotype of S^48-5

(Gaengel and Mlodzik, 2003)

NOT Enhancer of

Statement

Reference

spi¹/spi[+] is a non-enhancer of visible phenotype of vn^L6/vn¹

(Austin et al., 2014)

spi¹/spi[+] is a non-enhancer of neuroanatomy defective | third instar larval stage phenotype of Nf1^E2

(Walker et al., 2013)

spi¹/spi[+] is a non-enhancer of visible phenotype of Scer\GAL4^Tub.PU, csw^N308D.UASp

(Oishi et al., 2006)

spi¹ is a non-enhancer of visible phenotype of Scer\GAL4^ey.PH, brm^{K804R.UAS.Tag:HA}

(Armstrong et al., 2005)

spi¹ is a non-enhancer of visible phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Suppressor of

Statement

Reference

spi¹/spi[+] is a suppressor of increased cell number | third instar larval stage phenotype of Graf¹

(Kim et al., 2017)

spi¹ is a suppressor | partially of increased cell number | pupal stage phenotype of Vav²

(Martín-Bermudo et al., 2015)

spi¹ is a suppressor | partially of increased cell number | pupal stage phenotype of Vav³

(Martín-Bermudo et al., 2015)

spi¹/Krn²⁷ is a suppressor | partially of visible phenotype of AdamTS-B^KK108644, Scer\GAL4^Act5C.PU

(Butchar et al., 2012)

spi¹, vn^L6, Krn²⁷ is a suppressor of visible phenotype of AdamTS-B^KK108644, Scer\GAL4^Act5C.PU

(Butchar et al., 2012)

spi¹/spi[+] is a suppressor | partially of increased cell number | adult stage phenotype of sl²

(Murillo-Maldonado et al., 2011)

spi¹ is a suppressor of visible phenotype of Ret^MEN2B.GMR

(Read et al., 2005)

spi¹ is a suppressor of visible phenotype of Ret^MEN2A.GMR

(Read et al., 2005)

spi¹/spi[+] is a suppressor of visible phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, jing^UAS.cSa

(Sonnenfeld et al., 2004)

NOT Suppressor of

Statement

Reference

spi¹/spi[+] is a non-suppressor of neuroanatomy defective | third instar larval stage phenotype of Nf1^E2

(Walker et al., 2013)

spi¹ is a non-suppressor of visible phenotype of AdamTS-B^KK108644, Scer\GAL4^Act5C.PU

(Butchar et al., 2012)

spi¹/vn^L6 is a non-suppressor of visible phenotype of AdamTS-B^KK108644, Scer\GAL4^Act5C.PU

(Butchar et al., 2012)

spi¹/spi[+] is a non-suppressor of visible phenotype of Scer\GAL4^Tub.PU, csw^N308D.UASp

(Oishi et al., 2006)

spi¹ is a non-suppressor of visible phenotype of Scer\GAL4^ey.PH, brm^{K804R.UAS.Tag:HA}

(Armstrong et al., 2005)

spi¹ is a non-suppressor of visible phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

Other

Statement

Reference

Df(3L)Krn-27-7-B, Pvf1^EP1624, spi¹ has sterile phenotype

(McDonald et al., 2006)

Df(3L)Krn-27-7-B, Pvf1^EP1624, spi¹ has partially lethal phenotype

(McDonald et al., 2006)

jing³, spi¹/spi[+] has increased cell death | dominant phenotype

(Sonnenfeld et al., 2004)

jing[+]/jing³, spi¹ has increased cell death phenotype

(Sonnenfeld et al., 2004)

jing[+]/jing⁰¹⁰⁹⁴, spi¹ has neuroanatomy defective phenotype

(Sonnenfeld et al., 2004)

jing⁰¹⁰⁹⁴, spi¹/spi[+] has neuroanatomy defective | dominant phenotype

(Sonnenfeld et al., 2004)

Phenotype Manifest In

Enhanced by

Statement

Reference

spi¹ has denticle belt phenotype, enhanceable by vn^L6

(Austin et al., 2014)

spi¹, vn^L6 has denticle belt phenotype, enhanceable by Krn²⁷

(Austin et al., 2014)

Krn²⁷, spi¹ has denticle belt phenotype, enhanceable by vn^L6

(Austin et al., 2014)

spi¹ has denticle belt phenotype, enhanceable by Krn²⁷

(Austin et al., 2014)

Egfr^f1, spi¹ has somatic muscle | embryonic stage phenotype, enhanceable by S[+]/S^IIN

(Buff et al., 1998)

spi¹ has phenotype, enhanceable by vn^L6

(Schnepp et al., 1996)

spi¹ has phenotype, enhanceable by vn^ddd-4

(Schnepp et al., 1996)

NOT Enhanced by

Statement

Reference

Krn²⁷, spi¹, vn^L6 has denticle belt phenotype, non-enhanceable by grk^HF

(Austin et al., 2014)

Suppressed by

Statement

Reference

spi¹ has midline glial cell phenotype, suppressible by hid^rvX1/hid^rvX1

(Bergmann et al., 2002)

spi¹ has midline glial cell phenotype, suppressible | partially by rho^hs.PSt

(Lanoue and Jacobs, 1999)

NOT suppressed by

Statement

Reference

spi¹ has midline ventral glial cell phenotype, non-suppressible by jing^UAS.cSa/Scer\GAL4^sli.PS

(Sonnenfeld et al., 2004)

Enhancer of

Statement

Reference

spi¹/spi[+] is an enhancer of wing blade phenotype of sl²

(Murillo-Maldonado et al., 2011)

spi¹ is an enhancer of ommatidium phenotype of S^48-5

(Gaengel and Mlodzik, 2003)

spi¹ is an enhancer of interface glial cell phenotype of vn^γ4

(Hidalgo et al., 2001)

spi¹ is an enhancer of somatic muscle | embryonic stage phenotype of Egfr^f1, S^IIN

(Buff et al., 1998)

spi¹ is an enhancer of dorsal appendage phenotype of Ras85D^ix12a

(Wasserman and Freeman, 1998)

spi¹ is an enhancer of egg phenotype of Ras85D^ix12a

(Wasserman and Freeman, 1998)

spi¹ is an enhancer of phenotype of Egfr^E1

(Tio et al., 1994)

NOT Enhancer of

Statement

Reference

spi¹/spi[+] is a non-enhancer of wing vein L3 phenotype of vn^L6/vn¹

(Austin et al., 2014)

spi¹/spi[+] is a non-enhancer of NMJ bouton | supernumerary | third instar larval stage phenotype of Nf1^E2

(Walker et al., 2013)

spi¹/spi[+] is a non-enhancer of wing vein | ectopic phenotype of sl²

(Murillo-Maldonado et al., 2011)

spi¹ is a non-enhancer of border follicle cell phenotype of Pvf1^EP1624

(McDonald et al., 2006)

spi¹/spi[+] is a non-enhancer of wing vein | ectopic phenotype of Scer\GAL4^Tub.PU, csw^N308D.UASp

(Oishi et al., 2006)

spi¹ is a non-enhancer of eye phenotype of Scer\GAL4^ey.PH, brm^{K804R.UAS.Tag:HA}

(Armstrong et al., 2005)

spi¹ is a non-enhancer of eye phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

spi¹ is a non-enhancer of wing vein phenotype of vn¹

(Guichard et al., 1999)

Suppressor of

Statement

Reference

spi¹/spi[+] is a suppressor of hemocyte | supernumerary | third instar larval stage phenotype of Graf¹

(Kim et al., 2017)

spi¹ is a suppressor | partially of retina | pupal stage phenotype of Vav²

(Martín-Bermudo et al., 2015)

spi¹ is a suppressor | partially of cone cell | supernumerary | pupal stage phenotype of Vav²

(Martín-Bermudo et al., 2015)

spi¹ is a suppressor | partially of retina | pupal stage phenotype of Vav³

(Martín-Bermudo et al., 2015)

spi¹ is a suppressor | partially of cone cell | supernumerary | pupal stage phenotype of Vav³

(Martín-Bermudo et al., 2015)

spi¹/Krn²⁷ is a suppressor | partially of wing vein | ectopic phenotype of AdamTS-B^KK108644, Scer\GAL4^Act5C.PU

(Butchar et al., 2012)

spi¹, vn^L6, Krn²⁷ is a suppressor of wing vein | ectopic phenotype of AdamTS-B^KK108644, Scer\GAL4^Act5C.PU

(Butchar et al., 2012)

spi¹/spi[+] is a suppressor | partially of photoreceptor cell R7 | adult stage phenotype of sl²

(Murillo-Maldonado et al., 2011)

spi¹/Scer\GAL4^Tub.PU is a suppressor | partially of wing vein phenotype of Scer\GAL4^Tub.PU, csw^Y279C.UASp

(Oishi et al., 2009)

spi¹ is a suppressor of eye phenotype of Ret^MEN2B.GMR

(Read et al., 2005)

spi¹ is a suppressor of eye phenotype of Ret^MEN2A.GMR

(Read et al., 2005)

spi¹/spi[+] is a suppressor of ommatidium phenotype of jing^UAS.cSa

(Sonnenfeld et al., 2004)

spi¹/spi¹ is a suppressor of midline ventral glial cell | ectopic phenotype of Scer\GAL4^sli.PS, jing^UAS.cSa

(Sonnenfeld et al., 2004)

spi¹ is a suppressor of phenotype of arm³

(Cox et al., 2000)

spi¹ is a suppressor of dorsal appendage phenotype of rho^hs.PSt

(Wasserman and Freeman, 1998)

spi¹ is a suppressor of egg phenotype of rho^hs.PSt

(Wasserman and Freeman, 1998)

spi¹ is a suppressor of phenotype of rho^hs.sev

(Freeman, 1994)

spi¹ is a suppressor of phenotype of Egfr^E3

(Freeman, 1994)

spi¹ is a suppressor of phenotype of S²¹⁸

(Freeman, 1994)

NOT Suppressor of

Statement

Reference

spi¹ is a non-suppressor of primary pigment cell | supernumerary | pupal stage phenotype of Vav²

(Martín-Bermudo et al., 2015)

spi¹ is a non-suppressor of primary pigment cell | supernumerary | pupal stage phenotype of Vav³

(Martín-Bermudo et al., 2015)

spi¹/spi[+] is a non-suppressor of NMJ bouton | supernumerary | third instar larval stage phenotype of Nf1^E2

(Walker et al., 2013)

spi¹ is a non-suppressor of wing vein | ectopic phenotype of AdamTS-B^KK108644, Scer\GAL4^Act5C.PU

(Butchar et al., 2012)

spi¹/vn^L6 is a non-suppressor of wing vein | ectopic phenotype of AdamTS-B^KK108644, Scer\GAL4^Act5C.PU

(Butchar et al., 2012)

spi¹/spi[+] is a non-suppressor of wing vein | ectopic phenotype of Scer\GAL4^Tub.PU, csw^N308D.UASp

(Oishi et al., 2006)

spi¹ is a non-suppressor of eye phenotype of Scer\GAL4^ey.PH, brm^{K804R.UAS.Tag:HA}

(Armstrong et al., 2005)

spi¹/spi[+] is a non-suppressor of midline ventral glial cell | ectopic phenotype of Scer\GAL4^sli.PS, jing^UAS.cSa

(Sonnenfeld et al., 2004)

spi¹ is a non-suppressor of eye phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR

(Sullivan and Rubin, 2002)

spi¹ is a non-suppressor of phenotype of Src42A^Su(Raf)1-1

(Zhang et al., 1999)

Other

Statement

Reference

Df(3L)Krn-27-7-B, grk^unspecified, spi¹ has germarium phenotype

(Liu et al., 2010)

Df(3L)Krn²⁶⁰, spi¹ has photoreceptor cell R8 | somatic clone | third instar larval stage phenotype

(Brown et al., 2007)

Pvf1^EP1624, grk^HF, spi¹ has egg chamber phenotype

(McDonald et al., 2006)

jing³, spi¹/spi[+] has embryonic/larval dorsal trunk phenotype

(Sonnenfeld et al., 2004)

jing³, spi¹ has embryonic/larval dorsal trunk phenotype

(Sonnenfeld et al., 2004)

jing⁰¹⁰⁹⁴, spi¹ has midline ventral glial cell phenotype

(Sonnenfeld et al., 2004)

jing⁰¹⁰⁹⁴, spi¹/spi[+] has midline ventral glial cell phenotype

(Sonnenfeld et al., 2004)

da², spi¹/spi[+] has follicle cell phenotype

(Smith et al., 2002)

da², spi¹ has follicle cell phenotype

(Smith et al., 2002)

spi¹, vn^unspecified has longitudinal connective phenotype

(Lanoue et al., 2000)

spi¹, vn^unspecified has ventral nerve cord commissure phenotype

(Lanoue et al., 2000)

spi¹, vn^unspecified has ventral nerve cord | ventral phenotype

(Lanoue et al., 2000)

rho^hs.PSt, spi¹ has longitudinal connective phenotype

(Lanoue and Jacobs, 1999)

spi¹, vn^ddd-4 has embryonic/first instar larval cuticle phenotype

(Schnepp et al., 1996)

spi¹, vn^ddd-4 has denticle phenotype

(Schnepp et al., 1996)

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.

(Kim et al., 2017)

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.

(Martín-Bermudo et al., 2015)

vn^L6 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 grk^HF 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 vn^L6, with embryos having no denticle belts and a large anterior hole. A zygotic grk^HF mutation has no additional effect.

Krn²⁷/Krn⁹ enhances the wing vein phenotypes seen in vn^L6/vn¹ mutants. A greater proportion of flies show longitudinal vein 3 loss than in vn^L6/vn¹ alone. The phenotype is further enhanced by one copy of spi¹.

One copy of spi¹ does not enhance the vein phenotypes seen in vn^L6/vn¹ mutant wings.

(Austin et al., 2014)

The increase in mean number of boutons per neuromuscular junction which is seen in Nf1^E2 third instar larvae is not suppressed by spi¹/+.

(Walker et al., 2013)

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 spi¹.

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 spi¹.

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 spi¹ and Krn²⁷. The suppression is more pronounced if the flies simultaneously carry spi¹, Krn²⁷ and vn^L6.

(Butchar et al., 2012)

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.

(Jiang et al., 2011)

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.

(Murillo-Maldonado et al., 2011)

Germaria with germ line double mutant for grk^unspecified and spi¹ do not exhibit ectopic spectrosome containing cells.

Germaria with germ line triple mutant for Df(3L)Krn-27-7-B, grk^unspecified and spi¹ exhibit ectopic spectrosome containing cells.

(Liu et al., 2010)

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.

(Jiang and Edgar, 2009)

The presence of a spi¹ background causes minor suppression of ectopic wing vein formation found in csw^{Y279C.Scer\UAS} (Scer\GAL4^tub) mutants.

(Oishi et al., 2009)

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.

(Brown et al., 2007)

Pvf1^EP1624; spi¹ double mutant egg chambers show no enhancement of the border cell migration defects seen in Pvf1^EP1624 single mutants.

Pvf1^EP1624; spi¹; Df(3L)Krn-27-7-B triple mutants are poorly viable or sterile.

The egg chambers of Pvf1^EP1624; spi¹; grk^HF females do not develop normally.

(McDonald et al., 2006)

Expression of CycE^Scer\UAS.cLa, under the control of Scer\GAL4^en-e16E, in spi¹ embryos increases cell death in the posterior compartment, relative to expression of CycE^Scer\UAS.cLa in a wild-type background.

(Parker, 2006)

The increase in the number of midline glia per ventral nerve cord segment seen in embryos expressing jing^Scer\UAS.cSa under the control of Scer\GAL4^sli.PS is not suppressed by spi¹, but expression of jing^Scer\UAS.cSa under the control of Scer\GAL4^sli.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 jing^Scer\UAS.cSa under the control of Scer\GAL4^GMR.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.

(Sonnenfeld et al., 2004)

S^48-5/spi¹ mutants show 40.04%+-3.7 misrotated ommatidia compared to 9.55%+-1.43 seen in S^48-5 mutants alone.

(Gaengel and Mlodzik, 2003)

The loss of midline glial (MG) cells in spi¹ homozygous embryos is suppressed by W^rvX1/W^rvX1. 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).

(Bergmann et al., 2002)

Weakly enhances the eye phenotype produced by activated arm constructs. (either arm^S44Y.GMR or arm^S56F.GMR).

(Freeman and Bienz, 2001)

The decrease in interface glial cell numbers and increase in interface glial cell apoptosis seen in vn^γ4/Df(3L)γ3 are both enhanced by spi¹/spi¹.

(Hidalgo et al., 2001)

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.

(Rusten et al., 2001)

spi¹ ; vn^unspecified 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 ; vn^unspecified 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. vn^unspecified homozygotes that are also heterozygous for spi¹ have a single fused commissure and variably reduced longitudinal connectives.

(Lanoue et al., 2000)

In vn¹ homozygotes, there is no exacerbation of the loss of vein phenotype within homozygous spi¹ clones in the wing.

(Guichard et al., 1999)

The ubiquitous expression of rho^hs.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 rho^hs.PSt is added to wild-type embryos). Commissure separation in rho^hs.PSt,spi¹ is not improved.

(Lanoue and Jacobs, 1999)

Does not suppress the ability of Src42A^Su(phl)1-1 to suppress the lethality of phl¹/Y flies.

(Zhang et al., 1999)

The mild Egfr^f1 muscle phenotype is not affected by one copy of spi¹ alone, but spi¹ shows additional enhancement of the muscle phenotype in combination with S^IIN.

(Buff et al., 1998)

Reduction in dose of spi rescues the rho^hs.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 Egfr^E3 rough eye phenotype; more ommatidia and increase in the size of the eye.

(Freeman, 1994)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

spi^S3384

(Schwarz et al., 2018)

Rescued by

spi¹/spi^SC1 is rescued by Scer\GAL4^da.G32/spi^UAS.cSa

(Miura et al., 2006)

spi¹/spi^SCP2 is rescued by Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF/spi^UAS.cSa/Scer\GAL4^hs.PB

(Huang et al., 1998)

spi¹/spi^SCP2 is rescued by Scer\GAL4^αTub84B.PP/spi^UAS.cSa/Scer\GAL4^hs.PB

(Huang et al., 1998)

spi¹ is rescued by spi^+t12.5

(Rutledge et al., 1992)

Partially rescued by

spi¹/spi³ is partially rescued by spi^hs.PG

(Guichard et al., 1999)

spi¹/spi^SCP2 is partially rescued by spi^UAS.cSa/Scer\GAL4^hs.PB

(Huang et al., 1998)

Not rescued by

spi¹/spi^SC1 is not rescued by spi^CS.m.UAS/Scer\GAL4^da.G32

(Miura et al., 2006)

Comments

Unlike spi^Scer\UAS.cSa; Scer\GAL4^da.G32, spi^{CS.m.Scer\UAS}; Scer\GAL4^da.G32 completely fails to rescue lethality due to spi¹/spi^SC1.

(Miura et al., 2006)

Animals heterozygous for spi^SCP2 and spi¹ which have been rescued by spi^Scer\UAS.cSa with Scer\GAL4^hs.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\GAL4^GMR.PF or in clones induced to produce Scer\GAL4^αTub84B.PP.

(Huang et al., 1998)

Images (0)

Mutant

Wild-type

Stocks (2)

1859

106536

Notes on Origin

Discoverer

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.

(Kim and Crews, 1993)

No interaction with P{sev-svp1} or P{sev-svp2} exists.

(Begemann et al., 1995)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (12)

Reported As

Symbol Synonym

spi-1

(Gaengel and Mlodzik, 2003)

spi1

(Salzer et al., 2010)

spi^-

(Lawrence et al., 2002)

spi¹

(Álvarez and Díaz-Benjumea, 2018, Schwarz et al., 2018, Kim et al., 2017, Zhu et al., 2017, Martín-Bermudo et al., 2015, Morante et al., 2013, Steinhauer et al., 2013, Walker et al., 2013, Butchar et al., 2012, Hwang and Rulifson, 2011, Murillo-Maldonado et al., 2011, Yu et al., 2010, Lachance et al., 2009, Oishi et al., 2009, Estes et al., 2008, Kim et al., 2007, Liu et al., 2006, Oishi et al., 2006, Parker, 2006)

spi^2A14

(Liu et al., 2010, McDonald et al., 2006, Cox et al., 2000, Yagi and Hayashi, 1997)

spi^2A

(Austin et al., 2014)

spi^A14

(Jiang et al., 2011, Jiang and Edgar, 2009, Mao and Freeman, 2009, Brown et al., 2006, Urban et al., 2004, Smith et al., 2002, Dequier et al., 2001, Wasserman et al., 2000, Nagaraj et al., 1999, Chen et al., 1998, Huang et al., 1998, Szuts et al., 1998, Wasserman and Freeman, 1998, Huang and Fischer-Vize, 1996, Begemann et al., 1995, Schweitzer et al., 1995, Edgar et al., 1994, Freeman, 1994)

spi^I

(Guichard et al., 1999)

spi^IIA14

(Maeda et al., 2007, del Alamo et al., 2002, Sapir et al., 1998, Andrew et al., 1997, Luer et al., 1997, Scholz et al., 1997, Scholz et al., 1997, Kuo et al., 1996, Schnepp et al., 1996, Therianos et al., 1995, Baumann and Skaer, 1993, Panzer et al., 1992, Rutledge et al., 1992, Klambt et al., 1991)

spi^IIA

(Alvarez et al., 2003, Wessells et al., 1999, Buff et al., 1998, Simcox, 1997, Warrior, 1994, Tearle and Nusslein-Volhard, 1987)

spitz^IIA

(Su et al., 1999, Skeath, 1998)

Name Synonyms

spitzA14

(Brown et al., 2007)

Secondary FlyBase IDs

References (100)

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