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General Information
Symbol
Dmel\enaGC5
Species
D. melanogaster
Name
FlyBase ID
FBal0043043
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Mutagen
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
Caused by aberration
Expression Data
Reporter Expression
Additional Information
Statement
Reference
 
Marker for
Reflects expression of
Reporter construct used in assay
Human Disease Associations
Disease Ontology (DO) Annotations
Models Based on Experimental Evidence ( 0 )
Disease
Evidence
References
Modifiers Based on Experimental Evidence ( 0 )
Disease
Interaction
References
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference
The ISNb motor axon shows a bypass phenotype (the ISNb axons fail to enter the ventral longitudinal muscle field and instead bypass along the ISN root) in 99% of hemisegments in enaGC1/enaGC5 embryos.
75% of zygotic enaGC5/enaGC1 mutant embryos have a wild-type cuticle, while 21% show puckering along the dorsal midline.
enaGC5 animals exhibit a weak ISNb bypass phenotype, seen in about 7% of hemisegments.
enaGC1/enaGC5 mutants exhibit approximately 2 defects in longitudinal axon guidance per animal. An average of 18% of segments show defects. No embryos exhibit defects in pCC/MP1.
enaGC5/enaGC8 and enaGC5/enaGC1 embryos show modest levels of midline crossing errors by axons in the central nervous system.
86% of ISNb axons show a bypass phenotype in enaGC1/enaGC5 embryos. This phenotype is partially suppressed by enaScer\UAS.cCa expressed under the control of Scer\GAL4neu. 29% of ISNb axons show a bypass phenotype in enaGC5/enaGC8 embryos. A small number of RP neurons follow an aberrant path within the central nervous system.
Lethal in combination with enaGC1.
Heterozygotes with enaGC8 have diffuse and loosely bundled longitudinal and commissural axon tracts and some also exhibit axon misguiding. Some homozygous embryos exhibit thinning of longitudinal connectives, increased number of axons exciting the CNS from the longitudinal axons or failure of commissural axons to separate into anterior and posterior axon bundles. The overall organisation of the PNS is disrupted, spacing and organisation of the neurons is irregular and some clusters of neurons are mislocalised.
External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement
Reference
NOT suppressed by
Statement
Reference
enaGC5/enaGC1 has neuroanatomy defective | embryonic stage phenotype, non-suppressible by Dab1/Dab[+]
Enhancer of
Statement
Reference
ena[+]/enaGC5 is an enhancer of neuroanatomy defective phenotype of DAAMEx68
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
ena[+]/enaGC5 is a non-suppressor of neuroanatomy defective | larval stage phenotype of Abl4/Abl1
Other
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference
ena[+]/enaGC5 is an enhancer of neuropil phenotype of DAAMEx68
ena[+]/enaGC5 is an enhancer of fascicle phenotype of DAAMEx68
ena[+]/enaGC5 is an enhancer of connective phenotype of DAAMEx68
ena[+]/enaGC5 is an enhancer of lateral longitudinal fascicle phenotype of DAAMEx68
ena[+]/enaGC5 is an enhancer of embryo phenotype of DAAMEx68
enaGC5 is an enhancer of intersegmental nerve | heat sensitive phenotype of Nl1N-ts1
robo[+], ena[+], enaGC5, robo15 is an enhancer of longitudinal connective phenotype of sli1
ena[+]/enaGC5 is an enhancer of longitudinal connective phenotype of robo15, sli[+]/sli1
Suppressor of
Statement
Reference
NOT Suppressor of
Statement
Reference
ena[+]/enaGC5 is a non-suppressor of NMJ bouton | supernumerary phenotype of Abl4/Abl1
Other
Additional Comments
Genetic Interactions
Statement
Reference
The penetrance of the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab1/Dab2 females and having Dab1 as the paternally derived copy of Dab) is decreased by enaGC5/+ to 26%. The severe ISNb bypass phenotype seen in enaGC1/enaGC5 embryos is not suppressed by Dab1/+.
The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl1/Abl4 larvae is not suppressed by enaGC5/+. The increased bouton number per muscle area that is seen at the neuromuscular junction of Abl1/Abl4 larvae is significantly suppressed by AbiKO/+. This suppression further increased if the flies are also carrying enaGC5/+.
An enaGC5 heterozygous background increases the proportion of DAAMEx68 mutant embryos that exhibit CNS defects.
Stage 15 transheterozygous Df(2R)en-SFX31/enaGC5 embryos exhibit defects in central nervous system scaffolding with gaps in longitudinal tracts, loss of posterior commissures, or fusion of commissures in about 74.5% of the segments. Stage 15 transheterozygous enE/enaGC5 embryos exhibit defects in central nervous system scaffolding with gaps in longitudinal tracts, loss of posterior commissures, or fusion of commissures in about 15.2% of the segments.
When enaGC5/enaGC1 and homozygous dock3 are combined only a mild additive effect is see on the longitudinal exon guidance phenotype.
Xenogenetic Interactions
Statement
Reference
Hsap\VASPScer\UAS.cADa partially rescues the lethality of enaGC1/enaGC5 flies when expressed under the control of Scer\GAL4e22c; 25-85% of flies are rescued depending on the Hsap\VASPScer\UAS.cADa line used.
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
References (19)