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General Information
Symbol
Dmel\enaGC1
Species
D. melanogaster
Name
FlyBase ID
FBal0043039
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

Cultured primary neurons derived from enaGC1 and enaGC1/ena23 embryos show a significant reduction in the number of filopodia compared to control neurons. Mean filopodium length is reduced compared to wild type in these neurons.

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.

ena23/enaGC1 and ena210/enaGC1 embryos have reduced longitudinal axons in the central nervous system.

Embryos that are both maternally and zygotically mutant for ena (ena23/enaGC1 embryos derived from females with homozygous ena23 germlines) proceed through gastrulation normally and have normal epithelial integrity. Segmental grooves are deeper than normal in these embryos and persist long after they should have regressed. The leading edge during dorsal closure is often uneven. Most of the embryos fail in head involution. Cells that should lead head involution appear to constrict far more than in wild type, nearly severing the head from the thorax.

Mature embryos that are both maternally and zygotically mutant for ena (ena23/enaGC1 embryos derived from females with homozygous ena23 germlines) show defects in the cuticle; 10% have a dorsal pucker, 37% have a hole in the head, 15% have both a dorsal pucker and a hole in the head and 28% have a large ventral hole.

Mature embryos that are both maternally and zygotically mutant for ena (ena210/enaGC1 embryos derived from females with homozygous ena210 germlines) show defects in the cuticle; 15% have a dorsal pucker, 36% have a hole in the head, 14% have both a dorsal pucker and a hole in the head and 7% have a large ventral hole.

75% of zygotic enaGC5/enaGC1 mutant embryos have a wild-type cuticle, while 21% show puckering along the dorsal midline.

Third larval instar single cell homozygous ddaE and vpda neuron clones show a significant decrease in the number of dendritic ends compared to control clones.

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/enaGC1 embryos show modest levels of midline crossing errors by axons in the central nervous system.

Most enaGC1/ena210 embryos only have mild defects in head involution.

In ena210/enaGC1 mutant embryos, axons in the central nervous system appear to be less tightly fasciculated and commissural bundles sometimes appear abnormal and wander between commissures. Also there are occasional errors in midline guidance, and axon pathways that do not normally cross the midline sometimes do.

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.

Lethal in combination with enaGC5, ena23 or ena210.

Heterozygotes with enaGC8 have diffuse and loosely bundled longitudinal and commissural axon tracts. 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 abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Dab1/Dab[+]

Suppressor of
Statement
Reference
Other
Phenotype Manifest In
Enhanced by
Statement
Reference

enaGC1/ena210 has commissure phenotype, enhanceable by robo[+]/robo14

enaGC1/ena210 has longitudinal connective phenotype, enhanceable by robo[+]/robo14

enaGC1/ena210 has pCC neuron phenotype, enhanceable by robo[+]/robo14

enaGC1/ena210 has central nervous system phenotype, enhanceable by robo[+]/robo14

NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference

enaGC1 is an enhancer of intersegmental nerve | heat sensitive phenotype of Nl1N-ts1

ena[+]/enaGC1 is an enhancer of photoreceptor cell R7 & axon phenotype of Lar5.5/Lar2127

robo[+], ena[+], enaGC1, robo15 is an enhancer of longitudinal connective phenotype of sli1

ena[+]/enaGC1 is an enhancer of longitudinal connective phenotype of robo15, sli[+]/sli1

NOT Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
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 enaGC1/+ to 36%.

The severe ISNb bypass phenotype seen in enaGC1/enaGC5 embryos is not suppressed by Dab1/+.

A enaGC1 background does not affect the Sema-1aScer\UAS.cYa overexpression-induced hyperfasciculation phenotype.

The pupal eye patterning defect phenotype caused by the expression of cindrdsRNA.PC.PD.Scer\UAS driven by Scer\GAL4GMR.PF is enhanced by enaGC1/+.

The Scer\GAL4elav-C155/DAAMC.Scer\UAS.P\T gain-of-function phenotype (i.e the appearance of thicker commissures and nerve roots) is suppressed by a enaGC1/+ background.

When enaGC5/enaGC1 and homozygous dock3 are combined only a mild additive effect is see on the longitudinal exon guidance phenotype.

arm8/Y ; enaGC1/enaGC1 embryos have strong defects in dorsal closure and head involution, with no change in the segment polarity phenotype compared to arm8/Y embryos.

The addition of robo4/+ to ena210/enaGC1 mutants causes striking defects in central nervous system axon guidance. The anterior and posterior commissures are significantly thicker. longitudinal connectives are reduced and are sometimes closer to the midline. Also the pCC neuron frequently crosses the midline (which is not seen in wild-type or in ena210/enaGC1 alone).

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 (21)