Allele Dmel\SNF4Aγ^loe

General Information
Symbol	Dmel\SNF4Aγ^loe	Species	D. melanogaster
Name		FlyBase ID	FBal0144604
Feature type	allele	Associated gene	Dmel\SNF4Aγ
Also Known As	loe

Allele class
Mutagen	P-element activity
Recent Updates
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FB2013_03
FB2013_02	Controlled Vocabulary Terms phototaxis defective eye vacuole
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
Mutagen	P-element activity (Tschaepe et al., 2002)
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 P{lacW} insertion is within exon 7 of the loeII transcript. (Tschaepe et al., 2002)
Caused by insertion	P{lacW}SNF4Aγ^loe (Tschaepe et al., 2002, Wentzell et al., 2012, Cook et al., 2012)
Cytology
Phenotypic Data
Phenotypic Class
	neuroanatomy defective (Cook et al., 2012) neuroanatomy defective \| adult stage (Wentzell et al., 2012) neuroanatomy defective \| third instar larval stage (Wentzell et al., 2012) phototaxis defective (Cook et al., 2012)
Phenotype Manifest In
	adult brain (Tschaepe et al., 2002, Wentzell et al., 2012) adult central complex (Tschaepe et al., 2002) adult central nervous system (Tschaepe et al., 2002) embryonic/larval brain \| third instar larval stage (Wentzell et al., 2012) eye (Cook et al., 2012) vacuole (Cook et al., 2012)
Detailed Description
	Statement Reference SNF4Aγ[loe] homo- and heterozygous mutants exhibit age-dependent degeneration of the nervous system. SNF4Aγ[loe] exhibit a mild rough eye phenotype. (Cook et al., 2012) SNF4Aγ[loe] mutant third instar larval brains show increased vacuolisation compared to controls. The phenotype is more severe in males than in females. An increased number of vacuoles is also seen in 4 day old adult flies. (Wentzell et al., 2012) Mutants exhibit severe vacuolisation of the central nervous system. The vacuolar pathology is most prominent around the central complex and the central parts of the brain. Neurons appear to undergo necrotic cell death. Mutants also have ~40% reduced levels of cholesterol ester. (Tschaepe et al., 2002)
External Data
Linkouts
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement Reference SNF4Aγ^loe has neuroanatomy defective \| adult stage phenotype, enhanceable by Appl^d (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective \| third instar larval stage phenotype, enhanceable by Scer\GAL4^Appl.G1a/Appl^sd.Scer\UAS (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective \| third instar larval stage phenotype, enhanceable by Scer\GAL4^Appl.G1a/Bace^{Scer\UAS.cCSa} (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective phenotype, enhanceable by Rho1^V14.Scer\UAS/Scer\GAL4^Appl.G1a (Cook et al., 2012) SNF4Aγ^loe has phototaxis defective phenotype, enhanceable by Rho1^V14.Scer\UAS/Scer\GAL4^Appl.G1a (Cook et al., 2012)
NOT Enhanced by
Statement Reference SNF4Aγ^loe has neuroanatomy defective phenotype, non-enhanceable by Cdc42³ (Cook et al., 2012) SNF4Aγ^loe has neuroanatomy defective phenotype, non-enhanceable by Rab5^k08230 (Cook et al., 2012)
Suppressed by
Statement Reference Appl^d, SNF4Aγ^loe has neuroanatomy defective \| third instar larval stage phenotype, suppressible \| partially by Scer\GAL4^Appl.G1a/Appl^{Scer\UAS.cCSa} (Wentzell et al., 2012) Hsap\APP^{s.β.Scer\UAS.T:Ivir\HA1}, SNF4Aγ^loe, Scer\GAL4^Appl.G1a has neuroanatomy defective \| third instar larval stage phenotype, suppressible by Hsap\BACE1^Scer\UAS.cGa (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective \| third instar larval stage phenotype, suppressible by Appl^{s.Scer\UAS.T:Ivir\HA1}/Scer\GAL4^Appl.G1a (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective \| third instar larval stage phenotype, suppressible by Hsap\APP^{695.Scer\UAS.Exel}/Scer\GAL4^Appl.G1a (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective \| third instar larval stage phenotype, suppressible by Hsap\APP^{s.α.Scer\UAS.T:Ivir\HA1}/Scer\GAL4^Appl.G1a (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective \| third instar larval stage phenotype, suppressible by kuz^Scer\UAS.cFa/Scer\GAL4^Appl.G1a (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective \| third instar larval stage phenotype, suppressible by Scer\GAL4^Appl.G1a/Appl^{Scer\UAS.cCSa} (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective \| third instar larval stage phenotype, suppressible by Scer\GAL4^Appl.G1a/Hsap\APP^{s.β.Scer\UAS.T:Ivir\HA1} (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective phenotype, suppressible by Fpps[+]/Fpps^k06103 (Cook et al., 2012) SNF4Aγ^loe has neuroanatomy defective phenotype, suppressible by Rho1^72F/Rho1[+] (Cook et al., 2012) SNF4Aγ^loe has phototaxis defective phenotype, suppressible by Rho1^72F/Rho1[+] (Cook et al., 2012)
NOT suppressed by
Statement Reference Appl^d, SNF4Aγ^loe has neuroanatomy defective \| third instar larval stage phenotype, non-suppressible by Appl^{s.Scer\UAS.T:Ivir\HA1}/Scer\GAL4^Appl.G1a (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective \| third instar larval stage phenotype, non-suppressible by Appl^{dAICD.Scer\UAS.T:Ivir\HA1}/Scer\GAL4^Appl.G1a (Wentzell et al., 2012) SNF4Aγ^loe has neuroanatomy defective phenotype, non-suppressible by Cdc42³ (Cook et al., 2012) SNF4Aγ^loe has neuroanatomy defective phenotype, non-suppressible by Rab5^k08230 (Cook et al., 2012)
Other
Statement Reference Rho1^72F/Rho1[+], SNF4Aγ^loe has long lived phenotype (Cook et al., 2012)
Phenotype Manifest In
Enhanced by
Statement Reference SNF4Aγ^loe has adult brain phenotype, enhanceable by Appl^d (Tschaepe et al., 2002, Wentzell et al., 2012) SNF4Aγ^loe has adult brain phenotype, enhanceable by Scer\GAL4^Appl.G1a/Hmgcr^{Scer\UAS.cvDa} (Tschaepe et al., 2002) SNF4Aγ^loe has embryonic/larval brain \| third instar larval stage phenotype, enhanceable by Scer\GAL4^Appl.G1a/Appl^sd.Scer\UAS (Wentzell et al., 2012) SNF4Aγ^loe has embryonic/larval brain \| third instar larval stage phenotype, enhanceable by Scer\GAL4^Appl.G1a/Bace^{Scer\UAS.cCSa} (Wentzell et al., 2012) SNF4Aγ^loe has vacuole phenotype, enhanceable by Rho1^V14.Scer\UAS/Scer\GAL4^Appl.G1a (Cook et al., 2012)
Suppressed by
Statement Reference Appl^d, SNF4Aγ^loe has embryonic/larval brain \| third instar larval stage phenotype, suppressible \| partially by Scer\GAL4^Appl.G1a/Appl^{Scer\UAS.cCSa} (Wentzell et al., 2012) Hsap\APP^{s.β.Scer\UAS.T:Ivir\HA1}, SNF4Aγ^loe, Scer\GAL4^Appl.G1a has embryonic/larval brain \| third instar larval stage phenotype, suppressible by Hsap\BACE1^Scer\UAS.cGa (Wentzell et al., 2012) SNF4Aγ^loe has adult brain phenotype, suppressible by Hmgcr^clb1 (Tschaepe et al., 2002) SNF4Aγ^loe has adult brain phenotype, suppressible by Hmgcr^clb2 (Tschaepe et al., 2002) SNF4Aγ^loe has embryonic/larval brain \| third instar larval stage phenotype, suppressible by Appl^{s.Scer\UAS.T:Ivir\HA1}/Scer\GAL4^Appl.G1a (Wentzell et al., 2012) SNF4Aγ^loe has embryonic/larval brain \| third instar larval stage phenotype, suppressible by Hsap\APP^{695.Scer\UAS.Exel}/Scer\GAL4^Appl.G1a (Wentzell et al., 2012) SNF4Aγ^loe has embryonic/larval brain \| third instar larval stage phenotype, suppressible by Hsap\APP^{s.α.Scer\UAS.T:Ivir\HA1}/Scer\GAL4^Appl.G1a (Wentzell et al., 2012) SNF4Aγ^loe has embryonic/larval brain \| third instar larval stage phenotype, suppressible by kuz^Scer\UAS.cFa/Scer\GAL4^Appl.G1a (Wentzell et al., 2012) SNF4Aγ^loe has embryonic/larval brain \| third instar larval stage phenotype, suppressible by Scer\GAL4^Appl.G1a/Appl^{Scer\UAS.cCSa} (Wentzell et al., 2012) SNF4Aγ^loe has embryonic/larval brain \| third instar larval stage phenotype, suppressible by Scer\GAL4^Appl.G1a/Hsap\APP^{s.β.Scer\UAS.T:Ivir\HA1} (Wentzell et al., 2012) SNF4Aγ^loe has vacuole phenotype, suppressible by Fpps[+]/Fpps^k03514 (Cook et al., 2012) SNF4Aγ^loe has vacuole phenotype, suppressible by Rho1^72F/Rho1[+] (Cook et al., 2012)
NOT suppressed by
Statement Reference Appl^d, SNF4Aγ^loe has embryonic/larval brain \| third instar larval stage phenotype, non-suppressible by Appl^{s.Scer\UAS.T:Ivir\HA1}/Scer\GAL4^Appl.G1a (Wentzell et al., 2012) SNF4Aγ^loe has embryonic/larval brain \| third instar larval stage phenotype, non-suppressible by Appl^{dAICD.Scer\UAS.T:Ivir\HA1}/Scer\GAL4^Appl.G1a (Wentzell et al., 2012)
NOT Enhancer of
Statement Reference SNF4Agamma[+]/SNF4Aγ^loe is a non-enhancer of eye phenotype of cathD¹ (Kuronen et al., 2009) SNF4Aγ^loe is a non-enhancer of eye phenotype of Rho1^V14.Scer\UAS, Scer\GAL4^GMR.PF (Cook et al., 2012) SNF4Aγ^loe is a non-enhancer of retina phenotype of Rho1^V14.Scer\UAS, Scer\GAL4^GMR.PF (Cook et al., 2012)
NOT Suppressor of
Statement Reference SNF4Aγ^loe is a non-suppressor of eye phenotype of Rho1^V14.Scer\UAS, Scer\GAL4^GMR.PF (Cook et al., 2012) SNF4Aγ^loe is a non-suppressor of retina phenotype of Rho1^V14.Scer\UAS, Scer\GAL4^GMR.PF (Cook et al., 2012)
Additional Comments
Genetic Interactions
Statement Reference A Fpps[k06103] heterozygous background significantly suppresses the degenerative nervous sytem phenotype found in 5 day old SNF4Aγ[loe] mutants. These flies exhibit a reduction in the area of vacuoles in the optic system, from approximately 163 υm[2] to 33υm[2] in a Fpps[k03514]/+ background and 25υm[2] in a Fpps[k06103]/+ background. There is a similar reduction in the number of vacuoles present, confirming an involvement of the isoprenoid pathway in the degenerative phenotype of SNF4Aγ[loe] flies. There is no significant difference in the nervous system degeneration seen in SNF4Aγ[loe] mutants in a Cdc42[3] or Rab5[k08230] heterozygous background. A heterozygous Rho1[72F] background suppresses the neuronal vacuolization seen in SNF4Aγ[loe] mutants to approximately half the level in single mutants. The number of vacuoles is also reduced, compared to SNF4Aγ[loe] single mutants. Rho1[72F] heterozygosity increases the performance index of SNF4Aγ[loe] flies in a fast phototaxis assay. Expression of constitutively-active Rho1[V14.Scer\UAS] pan-neuronally, under the control of Scer\GAL4[Appl.G1a], enhances the neural degeneration and vacuolization seen in SNF4Aγ[loe] mutants. Expression of Rho1[V14.Scer\UAS] under the control of Scer\GAL4[Appl.G1a] decreases the performance index of SNF4Aγ[loe] flies in a fast phototaxis assay. A SNF4Aγ[loe] mutant background does not affect the external or internal eye phenotype caused by overexpression of Rho1[V14.Scer\UAS] under the control of Scer\GAL4[GMR.PF]. Rho1[72F]/+; SNF4Aγ[loe]/SNF4Aγ[loe] flies show a significant increase in lifespan compared to SNF4Aγ[loe] mutants. (Cook et al., 2012) Expression of Appl[Scer\UAS.cCSa] under the control of Scer\GAL4[Appl.G1a] substantially suppresses the increase in vacuolisation seen in the brains of SNF4Aγ[loe] mutant third instar larvae. Expression of Appl[s.Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[Appl.G1a] substantially suppresses the increase in vacuolisation seen in the brains of SNF4Aγ[loe] mutant third instar larvae. Expression of Appl[dAICD.Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[Appl.G1a] is unable to suppress the increase in vacuolisation seen in the brains of SNF4Aγ[loe] mutant third instar larvae. Expression of Appl[sd.Scer\UAS] under the control of Scer\GAL4[Appl.G1a] significantly enhances the increase in vacuolisation seen in the brains of SNF4Aγ[loe] mutant third instar larvae. Expression of Bace[Scer\UAS.cCSa] under the control of Scer\GAL4[Appl.G1a] enhances the increase in vacuolisation seen in the brains of SNF4Aγ[loe] mutant third instar larvae. Expression of kuz[Scer\UAS.cFa] under the control of Scer\GAL4[Appl.G1a] suppresses the increase in vacuolisation seen in the brains of SNF4Aγ[loe] mutant third instar larvae. Hemizygosity for Appl[d] enhances the vacuolisation seen in 4 day old SNF4Aγ[loe] mutant males. Expression of Appl[Scer\UAS.cCSa] under the control of Scer\GAL4[Appl.G1a] partially suppresses the vacuolisation seen in 4 day old Appl[d] SNF4Aγ[loe] double mutant males, returning the phenotype to the level seen in SNF4Aγ[loe] single mutants. Expression of Appl[s.Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[Appl.G1a] fails to suppress the vacuolisation seen in 4 day old Appl[d] SNF4Aγ[loe] double mutant males. (Wentzell et al., 2012) The addition of Hmgcr^clb1 or Hmgcr^clb2 to SNF4Aγ^loe animals shows a small but significant reduction in the number of holes seen in the adult brain. The addition of Hmgcr^{Scer\UAS.cvDa} (driven by Scer\GAL4^Appl.G1a) enhances the adult brain degeneration phenotype seen in SNF4Aγ^loe animals. The addition of Appl^d enhances the adult brain degeneration phenotype seen in SNF4Aγ^loe animals. (Tschaepe et al., 2002)
Xenogenetic Interactions
Statement Reference Expression of Hsap\APP[695.Scer\UAS.Exel] under the control of Scer\GAL4[Appl.G1a] dramatically suppresses the increase in vacuolisation seen in the brains of SNF4Aγ[loe] mutant third instar larvae. Expression of Hsap\APP[s.α.Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[Appl.G1a] fails to suppress the increase in vacuolisation seen in the brains of SNF4Aγ[loe] mutant third instar larvae. Expression of Hsap\APP[s.β.Scer\UAS.T:Ivir\HA1] under the control of Scer\GAL4[Appl.G1a] fails to suppress the increase in vacuolisation seen in the brains of SNF4Aγ[loe] mutant third instar larvae. Co-expression of Hsap\BACE1[Scer\UAS.cGa] suppresses the increase in vacuolisation seen when Hsap\APP[695.Scer\UAS.Exel] is expressed in the brains of SNF4Aγ[loe] mutant third instar larvae under the control of Scer\GAL4[Appl.G1a]. (Wentzell et al., 2012)
Complementation & Rescue Data
Rescued by	SNF4Aγ^loe is rescued by SNF4Aγ^{loeI.Scer\UAS}/Scer\GAL4^elav.PLu (Tschaepe et al., 2002)
Partially rescued by	SNF4Aγ^loe is partially rescued by SNF4Aγ^{Δ1-319.loeI.Scer\UAS}/Scer\GAL4^elav.PLu (Tschaepe et al., 2002) SNF4Aγ^loe is partially rescued by SNF4Aγ^{Δ1-738.loeI.Scer\UAS}/Scer\GAL4^elav.PLu (Tschaepe et al., 2002)
Not rescued by	SNF4Aγ^loe is not rescued by SNF4Aγ^{loeII.Scer\UAS}/Scer\GAL4^elav.PLu (Tschaepe et al., 2002)
Comments
Stocks ( 1 )
Bloomington	27905 w^*; P{UAS-Glaz.W}2; SNF4Aγ^loe/TM6B, Tb¹
Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	loe (Tschaepe et al., 2002, Wentzell et al., 2012) SNF4^loe (Kuronen et al., 2009) SNF4Aγ^loe
Name Synonym
Secondary FlyBase IDs

References ( 4 )
Research paper	Cook et al., 2012, PLoS ONE 7(9): e44440 Increased RhoA Prenylation in the loechrig (loe) Mutant Leads to Progressive Neurodegeneration. [FBrf0219441] Wentzell et al., 2012, Neurobiol. Disease 46(1): 78--87 Amyloid precursor proteins are protective in Drosophila models of progressive neurodegeneration. [FBrf0217742] Kuronen et al., 2009, Neurobiol. Disease 36(3): 488--493 Genetic modifiers of degeneration in the cathepsin D deficient Drosophila model for neuronal ceroid lipofuscinosis. [FBrf0209200] Tschaepe et al., 2002, EMBO J. 21(23): 6367--6376 The neurodegeneration mutant lochrig interferes with cholesterol homeostasis and APPL processing. [FBrf0155731]

Allele Dmel\SNF4Aγloe

Allele Dmel\SNF4Aγ^loe