FlyBase Allele Report: Dmel\ena[GC1]

Cultured primary neurons derived from ena^GC1 and ena^GC1/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.

(Gonçalves-Pimentel et al., 2011)

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.

(Song et al., 2010)

ena²³/ena^GC1 and ena²¹⁰/ena^GC1 embryos have reduced longitudinal axons in the central nervous system.

Embryos that are both maternally and zygotically mutant for ena (ena²³/ena^GC1 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/ena^GC1 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/ena^GC1 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 ena^GC5/ena^GC1 mutant embryos have a wild-type cuticle, while 21% show puckering along the dorsal midline.

(Gates et al., 2007)

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.

(Li et al., 2005)

ena^GC1/ena^GC5 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.

(Fan et al., 2003)

ena^GC5/ena^GC1 embryos show modest levels of midline crossing errors by axons in the central nervous system.

(Wills et al., 2002)

Most ena^GC1/ena²¹⁰ embryos only have mild defects in head involution.

(Grevengoed et al., 2001)

In ena²¹⁰/ena^GC1 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.

(Bashaw et al., 2000)

86% of ISNb axons show a bypass phenotype in ena^GC1/ena^GC5 embryos. This phenotype is partially suppressed by ena^Scer\UAS.cCa expressed under the control of Scer\GAL4^neu.

(Wills et al., 1999)

Lethal in combination with ena^GC5, ena²³ or ena²¹⁰.

(Ahern-Djamali et al., 1998)

Heterozygotes with ena^GC8 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.

(Gertler et al., 1995)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

ena^GC5/ena^GC1 has lethal phenotype, suppressible | partially by Hsap\VASP^UAS.cADa/Scer\GAL4^e22c

(Ahern-Djamali et al., 1998)

NOT suppressed by

Statement

Reference

ena^GC5/ena^GC1 has abnormal neuroanatomy | embryonic stage phenotype, non-suppressible by Dab¹/Dab[+]

(Song et al., 2010)

Suppressor of

Statement

Reference

ena[+]/ena^GC1 is a suppressor | partially of abnormal neuroanatomy | maternal effect | embryonic stage phenotype of Dab²/Dab¹

(Song et al., 2010)

ena[+]/ena^GC1 is a suppressor of abnormal neuroanatomy phenotype of DAAM^C.UASp

(Matusek et al., 2008)

Other

Statement

Reference

Hsap\VASP^UAS.cADa, Scer\GAL4^e22c, ena^GC5/ena^GC1 has viable phenotype

(Ahern-Djamali et al., 1998)

Phenotype Manifest In

Enhanced by

Statement

Reference

ena^GC1/ena²¹⁰ has symmetrical commissure phenotype, enhanceable by robo[+]/robo1⁴

(Bashaw et al., 2000)

ena^GC1/ena²¹⁰ has larval longitudinal connective phenotype, enhanceable by robo[+]/robo1⁴

(Bashaw et al., 2000)

ena^GC1/ena²¹⁰ has pCC neuron phenotype, enhanceable by robo[+]/robo1⁴

(Bashaw et al., 2000)

ena^GC1/ena²¹⁰ has central nervous system phenotype, enhanceable by robo[+]/robo1⁴

(Bashaw et al., 2000)

NOT suppressed by

Statement

Reference

ena^GC5/ena^GC1 has larval intersegmental nerve branch ISNb of A1-7 phenotype, non-suppressible by Dab¹/Dab[+]

(Song et al., 2010)

Enhancer of

Statement

Reference

ena[+]/ena^GC1 is an enhancer of eye | pupal stage phenotype of Scer\GAL4^GMR.PF, cindr^{RNAi.PC.PD.UAS}

(Johnson and Cagan, 2009)

ena^GC1 is an enhancer of larval intersegmental nerve | heat sensitive phenotype of N^l1N-ts1

(Crowner et al., 2003)

ena[+]/ena^GC1 is an enhancer of photoreceptor cell R7 & axon phenotype of Lar^5.5/Lar²¹²⁷

(Maurel-Zaffran et al., 2001)

robo[+], ena[+], ena^GC1, robo1⁵ is an enhancer of larval longitudinal connective phenotype of sli¹

(Bashaw et al., 2000)

ena[+]/ena^GC1 is an enhancer of larval longitudinal connective phenotype of robo1⁵, sli[+]/sli¹

(Bashaw et al., 2000)

NOT Enhancer of

Statement

Reference

ena[+]/ena^GC1 is a non-enhancer of larval longitudinal connective phenotype of Abl^EP3101, Scer\GAL4^elav.PLu

(Bashaw et al., 2000)

Suppressor of

Statement

Reference

ena[+]/ena^GC1 is a suppressor | partially of larval intersegmental nerve branch ISNb of A1-7 | maternal effect phenotype of Dab²/Dab¹

(Song et al., 2010)

ena[+]/ena^GC1 is a suppressor of fascicle | embryonic stage phenotype of DAAM^C.UASp, Scer\GAL4^elav-C155

(Matusek et al., 2008)

ena[+]/ena^GC1 is a suppressor of symmetrical commissure | embryonic stage phenotype of DAAM^C.UASp, Scer\GAL4^elav-C155

(Matusek et al., 2008)

ena^GC1 is a suppressor of symmetrical commissure phenotype of comm¹

(Bashaw et al., 2000)

ena^GC1 is a suppressor of symmetrical commissure phenotype of Scer\GAL4^unspecified, robo2^EP

(Bashaw et al., 2000)

ena[+]/ena^GC1 is a suppressor of symmetrical commissure phenotype of Scer\GAL4^unspecified, robo1^Y-F.UAS

(Bashaw et al., 2000)

ena^GC1 is a suppressor of symmetrical commissure phenotype of Scer\GAL4^unspecified, fra::robo1^{UAS.FR.Tag:MYC}

(Bashaw et al., 2000)

ena^GC1 is a suppressor | partially of larval ventral nerve cord commissure phenotype of Scer\GAL4^elav.PLu, robo2^UAS.cSa

(Simpson et al., 2000)

NOT Suppressor of

Statement

Reference

ena^GC1 is a non-suppressor of eye photoreceptor cell | third instar larval stage phenotype of Scer\GAL4^GMR.PF, Sema1a^UAS.cYa

(Yu et al., 2010)

ena^GC1 is a non-suppressor of lamina | third instar larval stage phenotype of Scer\GAL4^GMR.PF, Sema1a^UAS.cYa

(Yu et al., 2010)

Other

Statement

Reference

arm⁸, ena^GC1 has embryo | dorsal closure stage phenotype

(Grevengoed et al., 2001)

arm⁸, ena^GC1 has embryo | embryonic stage 14 phenotype

(Grevengoed et al., 2001)

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 ena^GC1/+ to 36%.

The severe ISNb bypass phenotype seen in ena^GC1/ena^GC5 embryos is not suppressed by Dab¹/+.

(Song et al., 2010)

A ena^GC1 background does not affect the Sema-1a^Scer\UAS.cYa overexpression-induced hyperfasciculation phenotype.

(Yu et al., 2010)

The pupal eye patterning defect phenotype caused by the expression of cindr^{dsRNA.PC.PD.Scer\UAS} driven by Scer\GAL4^GMR.PF is enhanced by ena^GC1/+.

(Johnson and Cagan, 2009)

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.

(Matusek et al., 2008)

When ena^GC5/ena^GC1 and homozygous dock³ are combined only a mild additive effect is see on the longitudinal exon guidance phenotype.

(Fan et al., 2003)

arm⁸/Y ; ena^GC1/ena^GC1 embryos have strong defects in dorsal closure and head involution, with no change in the segment polarity phenotype compared to arm⁸/Y embryos.

(Grevengoed et al., 2001)

The addition of robo⁴/+ to ena²¹⁰/ena^GC1 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/ena^GC1 alone).

(Bashaw et al., 2000)

Xenogenetic Interactions

Statement

Reference

Hsap\VASP^{Scer\UAS.cADa} partially rescues the lethality of ena^GC1/ena^GC5 flies when expressed under the control of Scer\GAL4^e22c; 25-85% of flies are rescued depending on the Hsap\VASP^{Scer\UAS.cADa} line used.

(Ahern-Djamali et al., 1998)

Complementation and Rescue Data

Fails to complement

ena^C14-06

(Sano et al., 2012)

Partially rescued by

ena^GC5/ena^GC1 is partially rescued by Scer\GAL4^neu/ena^{UAS.Tag:polyHis}

(Wills et al., 1999)

ena^GC5/ena^GC1 is partially rescued by Scer\GAL4^e22c/ena^UAS.cADa

(Ahern-Djamali et al., 1998)

ena^GC5/ena^GC1 is partially rescued by ena^K636stop.UAS/Scer\GAL4^e22c

(Ahern-Djamali et al., 1998)

ena^GC5/ena^GC1 is partially rescued by Scer\GAL4^e22c/ena^{UAS.Tag:polyHis}

(Comer et al., 1998)

ena^GC5/ena^GC1 is partially rescued by Scer\GAL4^e22c/ena^{YF.UAS.Tag:polyHis}

(Comer et al., 1998)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

8569

Adh^fn6 pr¹ cn¹ ena^GC1/CyO

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

ena^GC1

(Sano et al., 2012, Gonçalves-Pimentel et al., 2011, Song et al., 2010, Yu et al., 2010, Johnson and Cagan, 2009, Matusek et al., 2008, Gates et al., 2007, Yang and Bashaw, 2006, Li et al., 2005)

enb^GC1

Name Synonyms

Secondary FlyBase IDs

References (21)

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