A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Dmel\spz2

General Information
SymbolDmel\spz2SpeciesD. melanogaster
NameFlyBase IDFBal0016060
Feature typealleleAssociated geneDmel\spz
Also Known Asspz197
Allele classamorphic allele - genetic evidence
Mutagenethyl methanesulfonate
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Description
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FB2013_03
FB2013_02
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Mutations Mapped to the Genome
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Associated Sequence Data
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DNA sequence
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Cytology
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Statement
Reference
spz[2] mutant embryos exhibit aberrant targeting by the SNa motor axons. spz[2] flies can barely walk.
Hemolymph clots from spz[2] third instar larvae show normal melanization.
Homozygous females produce dorsalised embryos.
Level of Drs induction of bacterially challenged mutants is lower than in wild type. Pattern of response of CecA1 and CecA2 parallels that of Drs. Dpt and Dro remain fully inducible and pattern of expression of AttA and Def in intermediate. Infection of spz4/spz2 mutants with A.fumigatus causes 3% survival 3 days postinfection, infection with E.coli causes 84% survival 3 days postinfection.
Injection of snkΔne.T:ea into the central region of homozygous embryos causes a dorsalized phenotype.
Perivitelline fluid from Tl and dl donors was capable of restoring polarized gastrulation movements and cuticular elements.
Embryos derived from spz2/spz3 females are weakly dorsalised at 18oC. The mesoderm and ventral furrow are reduced in size, and mesoderm only develops in the posterior part of the embryo.
Embryos derived from homozygous females are dorsalised.
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spz2 has increased cell death phenotype, non-enhanceable by NT141
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Reference
spz2 is a non-enhancer of increased cell death phenotype of NT141
spz2 is a non-enhancer of neuroanatomy defective phenotype of NT141
spz2 is a non-enhancer of visible phenotype of osGMR.PB
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Statement
Reference
spz2 is a non-suppressor of visible phenotype of osGMR.PB
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Statement
Reference
NT141, spz2 has segmental nerve phenotype, enhanceable by spz5e03444
NT141, spz2 has transverse nerve phenotype, enhanceable by spz5e03444
spz5e03444, spz2 has segmental nerve phenotype, enhanceable by NT141
spz5e03444, spz2 has transverse nerve phenotype, enhanceable by NT141
spz2 has segmental nerve phenotype, enhanceable by NT141/spz5e03444
spz2 has transverse nerve phenotype, enhanceable by NT141/spz5e03444
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Statement
Reference
spz2/NT141 is an enhancer of segmental nerve phenotype of spz5e03444
spz2/NT141 is an enhancer of transverse nerve phenotype of spz5e03444
spz2/spz5e03444 is an enhancer of segmental nerve phenotype of NT141
spz2/spz5e03444 is an enhancer of transverse nerve phenotype of NT141
spz2 is an enhancer of segmental nerve phenotype of NT141, spz5e03444
spz2 is an enhancer of transverse nerve phenotype of NT141, spz5e03444
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Statement
Reference
spz2 is a non-enhancer of eye phenotype of osGMR.PB
spz2 is a non-enhancer of segmental nerve phenotype of NT141
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Statement
Reference
spz2 is a non-suppressor of eye phenotype of osGMR.PB
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Statement
Reference
The SNa axonal phenotype of spz[2] NT1[41] double-mutant embryos is epistatic to spz. Levels of apoptosis increase in the CNS of spz[2] and Tl[r3]/Df(3R)ro80b mutant embryos, indicating that both spz and Tl are required for neuronal survival. Levels of apoptosis do not increase further in spz[2] NT1[41] double mutants (compared to spz[2] mutants). Whereas homozygous spz[2] flies can eclose as adults, the NT1[41] spz[2] double mutants are completely lethal (100% penetrance). The penetrance of both SNa and ISNb/d targeting defects increases in spz5[e03444] NT1[41] spz[2], compared to the double or single mutants. In the triple mutants, misrouting phenotypes can be very dramatic, and there are cases of loss of all ISNb/d motor axons (not seen in single mutants). Misrouting of the transverse nerve (TN) can be very dramatic in triple mutants, although milder effects in this nerve occur with comparable penetrance in all genotypes (~10%). Misroutings of ISN are negligible in single and double mutants, but they increase and can be dramatic in triple-mutant embryos (12.7%). NT1[41] spz5[e03444] / NT1[41] Df(3L)Exel6092 double mutant flies display a range of behavioral phenotypes including: inability to estimate the location of a petri dish rim, falling off a petri dish rim, sluggishness, inability to climb, and wobbling.
Perivitelline fluid from embryos laid by Tlrv13 spz4/Tlrv4 spz2 females does not show axis-inducing activity when injected into the perivitelline space of embryos derived from pip1/pip2 females. Perivitelline fluid from embryos laid by eaD3 spz4/ea1 spz2 females does not show axis-inducing activity when injected into the perivitelline space of embryos derived from pip1/pip2 females. Perivitelline fluid from embryos laid by eaD1 spz2/ea4 spz4 females shows axis-inducing activity when injected into the the perivitelline space of embryos derived from pip1/pip2 females.
The zygotic semi-lethality of cact7 homozygotes is not suppressed by spz2.
Double mutant combinations with eaD1 are strongly dorsalizing.
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Statement
Reference
The presence of one copy of spz[2] markedly reduces the number of flies with melanin deposits caused by expression of Hsap\CHMP2B[Intron5.Scer\UAS] under the control of Scer\GAL4[GMR.PF].
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Rescued by
Partially rescued by
spz2 is partially rescued by spzp4-8.20
spz2 is partially rescued by spzp4-8.23
spz2 is partially rescued by spzp4-8.24
spz2 is partially rescued by spzp4-8.29
spz2 is partially rescued by spzp4-11.5
spz2 is partially rescued by spzp4-11.6
spz2 is partially rescued by spzp4-11.27
spz2 is partially rescued by spzp4-11.32
Comments
Microinjection of purified spz2.1 protein into the perivitelline space of syncytial blastoderm stage embryos rescues embryonic phenotype: restores the ventrolateral pattern elements and normalises the dorsal-ventral axis of the recipient embryo.
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Bloomington
Kyoto
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