|Feature type||allele||Associated gene||Dmel\ena|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Caused by aberration|
|Phenotype Manifest In|
Cultured primary neurons derived from ena[GC1] and ena[GC1]/ena 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 ena[GC1]/ena[GC5] embryos.
ena/ena[GC1] and ena/ena[GC1] embryos have reduced longitudinal axons in the central nervous system. Embryos that are both maternally and zygotically mutant for ena (ena/ena[GC1] embryos derived from females with homozygous ena 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 (ena/ena[GC1] embryos derived from females with homozygous ena 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 (ena/ena[GC1] embryos derived from females with homozygous ena 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 ena[GC5]/ena[GC1] mutant embryos have a wild-type cuticle, while 21% show puckering along the dorsal midline.
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.
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.
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.
|NOT suppressed by|
ena[+]/enaGC1 is a suppressor | partially of neuroanatomy defective | maternal effect | embryonic stage phenotype of Dab2/Dab1
|Phenotype Manifest In|
|NOT suppressed by|
ena[+], enaGC1, Scer\GAL4GMR.PF is an enhancer of eye | pupal stage phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, cindrdsRNA.Scer\UAS
|NOT Enhancer of|
ena[+]/enaGC1 is a suppressor | partially of intersegmental nerve branch ISNb of A1-7 | maternal effect phenotype of Dab2/Dab1
ena[+]/enaGC1 is a suppressor of commissure | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155
ena[+]/enaGC1 is a suppressor of fascicle | embryonic stage phenotype of DAAMC.Scer\UAS.P\T, Scer\GAL4elav-C155
enaGC1 is a suppressor | partially of ventral nerve cord commissure phenotype of Scer\GAL4elav.PLu, leaScer\UAS.cSa
enaGC1 is a suppressor of commissure phenotype of Scer\GAL4unspecified, fra::roboScer\UAS.FR.T:Hsap\MYC
|NOT Suppressor of|
enaGC1 is a non-suppressor of eye photoreceptor cell | third instar larval stage phenotype of Scer\GAL4GMR.PF/Scer\GAL4GMR.PF, Sema-1aScer\UAS.cYa
The penetrance of the ISNb stall phenotype seen in embryos lacking both maternal and zygotic Dab function (derived from Dab/Dab females and having Dab as the paternally derived copy of Dab) is decreased by ena[GC1]/+ to 36%. The severe ISNb bypass phenotype seen in ena[GC1]/ena[GC5] embryos is not suppressed by Dab/+.
A ena[GC1] background does not affect the Sema-1a[Scer\UAS.cYa] overexpression-induced hyperfasciculation phenotype.
The pupal eye patterning defect phenotype caused by the expression of cindr[dsRNA.Scer\UAS] driven by Scer\GAL4[GMR.PF] is enhanced by ena[GC1]/+.
The Scer\GAL4[elav-C155]/DAAM[C.Scer\UAS.P\T] gain-of-function phenotype (i.e the appearance of thicker commissures and nerve roots) is suppressed by a ena[GC1]/+ 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).
|Complementation & Rescue Data|
|Fails to complement|
|Partially rescued by|
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 2 )|
|Secondary FlyBase IDs|
|References ( 19 )|