Allele Dmel\spi¹

General Information
Symbol	Dmel\spi¹	Species	D. melanogaster
Name		FlyBase ID	FBal0016005
Feature type	allele	Associated gene	Dmel\spi
Also Known As	spi^A14, spi^IIA14, spi^IIA, spi^2A14, spitz^IIA

Allele class	loss of function allele
Mutagen	ethyl methanesulfonate
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
Update Feed	Click the icon below to subscribe to this FlyBase record and receive updates automatically through your feed reader.
FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class	loss of function allele (Freeman, 1994)
Mutagen	ethyl methanesulfonate (Tearle and Nusslein-Volhard, 1987, Rutledge et al., 1992)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference
Cytology
Phenotypic Data
Phenotypic Class
	cell death defective \| somatic clone \| third instar larval stage (Brown et al., 2007) increased cell death (Urban et al., 2004) increased cell death \| embryonic stage (Parker, 2006) increased cell death \| somatic clone (Wasserman et al., 2000) neuroanatomy defective (Sonnenfeld et al., 2004) neuroanatomy defective \| embryonic stage (Sepp and Auld, 2003)
Phenotype Manifest In
	abdominal 2 dorsal acute muscle 1 (Buff et al., 1998, Su et al., 1999) abdominal 3 dorsal acute muscle 1 (Buff et al., 1998, Su et al., 1999) abdominal 4 dorsal acute muscle 1 (Buff et al., 1998, Su et al., 1999) abdominal 5 dorsal acute muscle 1 (Buff et al., 1998, Su et al., 1999) abdominal 6 dorsal acute muscle 1 (Buff et al., 1998, Su et al., 1999) abdominal 7 dorsal acute muscle 1 (Buff et al., 1998, Su et al., 1999) abdominal dorso-lateral adult muscle precursor cell (Figeac et al., 2010) abdominal lateral adult muscle precursor cell (Figeac et al., 2010) abdominal lateral pentascolopidial chordotonal organ lch5 (Elstob et al., 2001) adult salivary gland primordium (Panzer et al., 1992) anterior commissure (Klambt et al., 1991) anterior fascicle sensory neuron (Sepp and Auld, 2003) Bolwig organ (Daniel et al., 1999, Dumstrei et al., 1998) bract \| somatic clone (del Alamo et al., 2002) denticle belt (Urban et al., 2004) denticle belt \| ventral (Simcox, 1997) dorsal neurohemal organ (Luer et al., 1997) egg \| dorsal (Wasserman and Freeman, 1998) embryonic/first instar larval cuticle (Urban et al., 2004) embryonic/larval brain (Dumstrei et al., 1998) embryonic/larval oenocyte (Elstob et al., 2001, Rusten et al., 2001) embryonic/larval optic lobe \| posterior (Daniel et al., 1999) embryonic/larval recurrent nerve (Dumstrei et al., 1998) embryonic/larval somatic muscle (Buff et al., 1998) embryonic segment \| posterior compartment (Parker, 2006) embryonic stomatogastric nervous system (Dumstrei et al., 1998) embryonic ventral epidermis (Kim and Crews, 1993) eye disc \| somatic clone (Wasserman et al., 2000) hypocerebral ganglion (Dumstrei et al., 1998) lamina & neuron (Huang et al., 1998) lch5 neuron (Rusten et al., 2001) longitudinal connective (Lanoue et al., 2000) Malpighian tubule (Baumann and Skaer, 1993) midline glial cell (Bergmann et al., 2002, Lanoue and Jacobs, 1999, Lanoue et al., 2000, Luer et al., 1997, Klambt et al., 1991) midline ventral glial cell (Sonnenfeld et al., 2004) ommatidium (Tio and Moses, 1997) optic lobe (Dumstrei et al., 1998) peripheral glial cell \| embryonic stage (Sepp and Auld, 2003) photoreceptor cell R1 (Huang et al., 1998) photoreceptor cell R2 (Huang et al., 1998, Tio et al., 1994, Tio and Moses, 1997) photoreceptor cell R3 (Huang et al., 1998, Tio et al., 1994) photoreceptor cell R4 (Huang et al., 1998, Tio et al., 1994) photoreceptor cell R5 (Huang et al., 1998, Tio et al., 1994, Tio and Moses, 1997) photoreceptor cell R6 (Huang et al., 1998) photoreceptor cell R7 (Huang et al., 1998) photoreceptor cell R8 (Tio et al., 1994) posterior commissure (Klambt et al., 1991) posterior fascicle sensory neuron (Sepp and Auld, 2003) sensory neuron & axon & embryo (Sepp and Auld, 2003) ventral longitudinal muscle (Buff et al., 1998) ventral nerve cord \| dorsal (Lanoue et al., 2000) ventral nerve cord commissure (Lanoue et al., 2000) ventral oblique muscle (Buff et al., 1998)
Detailed Description
	Statement Reference 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 spi[1] have normal cardiac function. (Yu et al., 2010) The proliferation of spi[1] 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 somatic clones in the legs and wings have bractless mechanosensory bristles. (del Alamo et al., 2002) Homozygous clones in the adult abdomen do not show any consistent alterations of normal polarity. (Lawrence 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 the 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 cell polarity defective phenotype of S^48-5 (Gaengel and Mlodzik, 2003) spi¹ is an enhancer of increased cell death \| embryonic stage phenotype of CycE^Scer\UAS.cLa, Scer\GAL4^en-e16E (Parker, 2006)
NOT Enhancer of
Statement Reference spi¹/spi[+] is a non-enhancer of visible phenotype of Scer\GAL4^tub.PU, csw^{N308D.Scer\UAS.P\T} (Oishi et al., 2006) spi¹ is a non-enhancer of visible phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR (Sullivan and Rubin, 2002) spi¹ is a non-enhancer of visible phenotype of Scer\GAL4^ey.PH, brm^{K804R.Scer\UAS.T:Ivir\HA1} (Armstrong et al., 2005)
Suppressor of
Statement Reference spi¹, vn^L6, Krn²⁷ is a suppressor of visible phenotype of CG4096^KK108644, Scer\GAL4^Act5C.PU (Butchar et al., 2012) spi¹/Krn²⁷ is a suppressor \| partially of visible phenotype of CG4096^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/spi[+] is a suppressor of visible phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, jing^Scer\UAS.cSa (Sonnenfeld et al., 2004) spi¹ is a suppressor of visible phenotype of Ret^MEN2A.GMR (Read et al., 2005) spi¹ is a suppressor of visible phenotype of Ret^MEN2B.GMR (Read et al., 2005)
NOT Suppressor of
Statement Reference spi¹/spi[+] is a non-suppressor of visible phenotype of Scer\GAL4^tub.PU, csw^{N308D.Scer\UAS.P\T} (Oishi et al., 2006) spi¹/vn^L6 is a non-suppressor of visible phenotype of CG4096^KK108644, Scer\GAL4^Act5C.PU (Butchar et al., 2012) spi¹ is a non-suppressor of visible phenotype of CanB^GMR.PS, Pp2B-14D^act.GMR (Sullivan and Rubin, 2002) spi¹ is a non-suppressor of visible phenotype of CG4096^KK108644, Scer\GAL4^Act5C.PU (Butchar et al., 2012) spi¹ is a non-suppressor of visible phenotype of Scer\GAL4^ey.PH, brm^{K804R.Scer\UAS.T:Ivir\HA1} (Armstrong et al., 2005)
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 viable \| poor phenotype (McDonald et al., 2006) jing[+]/jing³, spi¹ has increased cell death phenotype (Sonnenfeld et al., 2004) jing[+]/jing⁰¹⁰⁹⁴, spi¹ has neuroanatomy defective phenotype (Sonnenfeld et al., 2004) jing³, spi¹/spi[+] has increased cell death \| dominant phenotype (Sonnenfeld et al., 2004) jing⁰¹⁰⁹⁴, spi¹/spi[+] has neuroanatomy defective \| dominant phenotype (Sonnenfeld et al., 2004)
Phenotype Manifest In
Enhanced by
Statement Reference Egfr^f1, spi¹ has somatic muscle \| embryonic stage phenotype, enhanceable by S[+]/S^IIN (Buff et al., 1998) spi¹ has phenotype, enhanceable by vn^ddd-4 (Schnepp et al., 1996) spi¹ has phenotype, enhanceable by vn^L6 (Schnepp et al., 1996)
Suppressed by
Statement Reference spi¹ has midline glial cell phenotype, suppressible \| partially by rho^hs.PSt (Lanoue and Jacobs, 1999) spi¹ has midline glial cell phenotype, suppressible by W^rvX1/W^rvX1 (Bergmann et al., 2002)
NOT suppressed by
Statement Reference spi¹ has midline ventral glial cell phenotype, non-suppressible by jing^Scer\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 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 embryonic segment \| posterior compartment phenotype of CycE^Scer\UAS.cLa, Scer\GAL4^en-e16E (Parker, 2006) spi¹ is an enhancer of interface glial cell phenotype of vn^γ4 (Hidalgo et al., 2001) spi¹ is an enhancer of ommatidium phenotype of S^48-5 (Gaengel and Mlodzik, 2003) spi¹ is an enhancer of phenotype of Egfr^E1 (Tio et al., 1994) spi¹ is an enhancer of somatic muscle \| embryonic stage phenotype of Egfr^f1, S^IIN (Buff et al., 1998)
NOT Enhancer of
Statement Reference spi¹/spi[+] is a non-enhancer of wing vein \| ectopic phenotype of Scer\GAL4^tub.PU, csw^{N308D.Scer\UAS.P\T} (Oishi et al., 2006) 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 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 eye phenotype of Scer\GAL4^ey.PH, brm^{K804R.Scer\UAS.T:Ivir\HA1} (Armstrong et al., 2005) spi¹ is a non-enhancer of wing vein phenotype of vn¹ (Guichard et al., 1999)
Suppressor of
Statement Reference spi¹, vn^L6, Krn²⁷ is a suppressor of wing vein \| ectopic phenotype of CG4096^KK108644, Scer\GAL4^Act5C.PU (Butchar et al., 2012) spi¹/Krn²⁷ is a suppressor \| partially of wing vein \| ectopic phenotype of CG4096^KK108644, Scer\GAL4^Act5C.PU (Butchar et al., 2012) spi¹/Scer\GAL4^tub.PU is a suppressor \| partially of wing vein phenotype of Scer\GAL4^tub.PU, csw^{Y279C.Scer\UAS.P\T} (Oishi et al., 2009) spi¹/spi[+] is a suppressor \| partially of photoreceptor cell R7 \| adult stage phenotype of sl² (Murillo-Maldonado et al., 2011) spi¹/spi[+] is a suppressor of ommatidium phenotype of jing^Scer\UAS.cSa (Sonnenfeld et al., 2004) spi¹/spi¹ is a suppressor of midline ventral glial cell \| ectopic phenotype of Scer\GAL4^sli.PS, jing^Scer\UAS.cSa (Sonnenfeld et al., 2004, Sonnenfeld et al., 2004) 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 eye phenotype of Ret^MEN2A.GMR (Read et al., 2005) spi¹ is a suppressor of eye phenotype of Ret^MEN2B.GMR (Read et al., 2005) spi¹ is a suppressor of phenotype of arm³ (Cox et al., 2000) spi¹ is a suppressor of phenotype of Egfr^E3 (Freeman, 1994) spi¹ is a suppressor of phenotype of rho^hs.sev (Freeman, 1994) spi¹ is a suppressor of phenotype of S²¹⁸ (Freeman, 1994)
NOT Suppressor of
Statement Reference spi¹/spi[+] is a non-suppressor of midline ventral glial cell \| ectopic phenotype of Scer\GAL4^sli.PS, jing^Scer\UAS.cSa (Sonnenfeld et al., 2004) spi¹/spi[+] is a non-suppressor of wing vein \| ectopic phenotype of Scer\GAL4^tub.PU, csw^{N308D.Scer\UAS.P\T} (Oishi et al., 2006) spi¹/vn^L6 is a non-suppressor of wing vein \| ectopic phenotype of CG4096^KK108644, Scer\GAL4^Act5C.PU (Butchar et al., 2012) 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 eye phenotype of Scer\GAL4^ey.PH, brm^{K804R.Scer\UAS.T:Ivir\HA1} (Armstrong et al., 2005) spi¹ is a non-suppressor of phenotype of Src42A^Su(phl)1-1 (Zhang et al., 1999) spi¹ is a non-suppressor of wing vein \| ectopic phenotype of CG4096^KK108644, Scer\GAL4^Act5C.PU (Butchar et al., 2012)
Other
Statement Reference da², spi¹/spi[+] has follicle cell phenotype (Smith et al., 2002) da², spi¹ has follicle cell phenotype (Smith et al., 2002) 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) 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/spi[+] has midline ventral glial cell phenotype (Sonnenfeld et al., 2004) jing⁰¹⁰⁹⁴, spi¹ has midline ventral glial cell phenotype (Sonnenfeld et al., 2004) Pvf1^EP1624, grk^HF, spi¹ has egg chamber phenotype (McDonald et al., 2006) rho^hs.PSt, spi¹ has longitudinal connective phenotype (Lanoue and Jacobs, 1999, Lanoue and Jacobs, 1999) spi¹, vn^ddd-4 has denticle phenotype (Schnepp et al., 1996) spi¹, vn^ddd-4 has embryonic/first instar larval cuticle phenotype (Schnepp et al., 1996) spi¹, vn^unspecified has longitudinal connective phenotype (Lanoue et al., 2000, Lanoue et al., 2000) spi¹, vn^unspecified has ventral nerve cord \| ventral phenotype (Lanoue et al., 2000, Lanoue et al., 2000) spi¹, vn^unspecified has ventral nerve cord commissure phenotype (Lanoue et al., 2000, Lanoue et al., 2000)
Additional Comments
Genetic Interactions
Statement Reference 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[1]. 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[1]. 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[1] and Krn[27]. The suppression is more pronounced if the flies simultaneously carry spi[1], Krn[27] and vn[L6]. (Butchar et al., 2012) One copy of spi[1] enhances the reduction in wing blade area seen in homozygous sl[2] males. One copy of spi[1] does not enhance the ectopic wing vein phenotype seen in sl[2] homozygotes. One copy of spi[1] partially suppresses the percentage of sl[2] 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 spi[1] do not exhibit ectopic spectrosome containing cells. Germaria with germ line triple mutant for Df(3L)Krn-27-7-B, grk[unspecified] and spi[1] exhibit ectopic spectrosome containing cells. (Liu et al., 2010) The proliferation of spi[1] 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 spi[1] background causes minor suppression of ectopic wing vein formation found in csw[Y279C.Scer\UAS] (Scer\GAL4[tub]) mutants. (Oishi et al., 2009) spi[1] clones made in the Df(3L)Krn[260] 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 & Rescue Data
Rescued by	spi¹/spi^SC1 is rescued by Scer\GAL4^da.G32/spi^Scer\UAS.cSa (Miura et al., 2006) spi¹/spi^SCP2 is rescued by Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF/spi^Scer\UAS.cSa/Scer\GAL4^hs.PB (Huang et al., 1998) spi¹/spi^SCP2 is rescued by Scer\GAL4^αTub84B.PP/spi^Scer\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^Scer\UAS.cSa/Scer\GAL4^hs.PB (Huang et al., 1998)
Not rescued by	spi¹/spi^SC1 is not rescued by spi^{CS.m.Scer\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)
Stocks ( 2 )
Bloomington	1859 spi¹ cn¹ bw¹ sp¹/CyO
Kyoto	106536 spi¹ cn¹ bw¹ sp¹/CyO
Notes on Origin
Discoverer

Comments
	No interaction with P{sev-svp1} or P{sev-svp2} exists. (Begemann et al., 1995) 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)
External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 11 )
Reported As
Symbol Synonym	spi-1 (Gaengel and Mlodzik, 2003) spi1 (Salzer et al., 2010) spi¹ (Parker, 2006, Liu et al., 2006, Butchar et al., 2012, Estes et al., 2008, Lachance et al., 2009, Oishi et al., 2009, Yu et al., 2010, Murillo-Maldonado et al., 2011, Oishi et al., 2006) spi^2A14 (Cox et al., 2000, Yagi and Hayashi, 1997, McDonald et al., 2006, Liu et al., 2010) spi^- (Lawrence et al., 2002) spi^A14 (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) spi^I (Guichard et al., 1999) spi^IIA14 (del Alamo et al., 2002, Sapir et al., 1998, Scholz et al., 1997, Luer et al., 1997, Scholz et al., 1997, Andrew et al., 1997, Schnepp et al., 1996, Kuo et al., 1996, Therianos et al., 1995, Baumann and Skaer, 1993, Rutledge et al., 1992, Panzer 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 Synonym	spitz^A14 (Brown et al., 2007)
Secondary FlyBase IDs

References ( 87 )

Generate a list of	All references relating to this allele ( 87 )

List References by type	Research paper ( 85 ) Erratum ( 1 ) Stock list ( 1 )
Recent research papers ( 2 )
	Butchar et al., 2012, Genetics 191(4): 1213--1226 New negative feedback regulators of egfr signaling in Drosophila. [FBrf0219175] Murillo-Maldonado et al., 2011, PLoS ONE 6(11): e28067 Insulin Receptor-Mediated Signaling via Phospholipase C-γ Regulates Growth and Differentiation in Drosophila. [FBrf0216849] Show all research papers ...

Allele Dmel\spi1

Allele Dmel\spi¹