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.
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.
enaGC5/enaGC1 has lethal phenotype, suppressible | partially by Hsap\VASPUAS.cADa/Scer\GAL4e22c
enaGC5/enaGC1 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Dab1/Dab[+]
ena[+]/enaGC1 is a suppressor | partially of abnormal neuroanatomy | maternal effect | embryonic stage phenotype of Dab2/Dab1
ena[+]/enaGC1 is a suppressor of abnormal neuroanatomy phenotype of DAAMC.UASp
Hsap\VASPUAS.cADa, Scer\GAL4e22c, enaGC5/enaGC1 has viable phenotype
enaGC1/ena210 has symmetrical commissure phenotype, enhanceable by robo[+]/robo14
enaGC1/ena210 has larval 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
enaGC5/enaGC1 has larval intersegmental nerve branch ISNb of A1-7 phenotype, non-suppressible by Dab1/Dab[+]
ena[+]/enaGC1 is an enhancer of eye | pupal stage phenotype of Scer\GAL4GMR.PF, cindrRNAi.PC.PD.UAS
enaGC1 is an enhancer of larval intersegmental nerve | heat sensitive phenotype of Nl1N-ts1
robo[+], ena[+], enaGC1, robo15 is an enhancer of larval longitudinal connective phenotype of sli1
ena[+]/enaGC1 is an enhancer of larval longitudinal connective phenotype of robo15, sli[+]/sli1
ena[+]/enaGC1 is a non-enhancer of larval longitudinal connective phenotype of AblEP3101, Scer\GAL4elav.PLu
ena[+]/enaGC1 is a suppressor | partially of larval intersegmental nerve branch ISNb of A1-7 | maternal effect phenotype of Dab2/Dab1
ena[+]/enaGC1 is a suppressor of fascicle | embryonic stage phenotype of DAAMC.UASp, Scer\GAL4elav-C155
ena[+]/enaGC1 is a suppressor of symmetrical commissure | embryonic stage phenotype of DAAMC.UASp, Scer\GAL4elav-C155
enaGC1 is a suppressor of symmetrical commissure phenotype of comm1
enaGC1 is a suppressor of symmetrical commissure phenotype of Scer\GAL4unspecified, robo2EP
ena[+]/enaGC1 is a suppressor of symmetrical commissure phenotype of Scer\GAL4unspecified, robo1Y-F.UAS
enaGC1 is a suppressor of symmetrical commissure phenotype of Scer\GAL4unspecified, fra::robo1UAS.FR.Tag:MYC
enaGC1 is a suppressor | partially of larval ventral nerve cord commissure phenotype of Scer\GAL4elav.PLu, robo2UAS.cSa
enaGC1 is a non-suppressor of eye photoreceptor cell | third instar larval stage phenotype of Scer\GAL4GMR.PF, Sema1aUAS.cYa
enaGC1 is a non-suppressor of lamina | third instar larval stage phenotype of Scer\GAL4GMR.PF, Sema1aUAS.cYa
arm8, enaGC1 has embryo | dorsal closure stage phenotype
arm8, enaGC1 has embryo | embryonic stage 14 phenotype
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.
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).
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.
enaGC5/enaGC1 is partially rescued by Scer\GAL4neu/enaUAS.Tag:polyHis
enaGC5/enaGC1 is partially rescued by Scer\GAL4e22c/enaUAS.cADa
enaGC5/enaGC1 is partially rescued by enaK636stop.UAS/Scer\GAL4e22c
enaGC5/enaGC1 is partially rescued by Scer\GAL4e22c/enaUAS.Tag:polyHis
enaGC5/enaGC1 is partially rescued by Scer\GAL4e22c/enaYF.UAS.Tag:polyHis