Allele Dmel\ena^GC1

General Information
Symbol	Dmel\ena^GC1	Species	D. melanogaster
Name		FlyBase ID	FBal0043039
Feature type	allele	Associated gene	Dmel\ena

Allele class
Mutagen	gamma ray
Recent Updates
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FB2013_03
FB2013_02
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Nature of the Allele
Allele class
Mutagen	gamma ray (Gertler et al., 1995)
Mutations Mapped to the Genome

Type Location Additional Notes References
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype
Nature of the lesion	Statement Reference
Caused by aberration	In(2R)ena^GC1 (Gertler et al., 1995, Fan et al., 2003)
Cytology
Phenotypic Data
Phenotypic Class
	lethal \| embryonic stage (with ena²³) (Gonçalves-Pimentel et al., 2011) lethal \| embryonic stage (with ena^GC5) (Gonçalves-Pimentel et al., 2011) lethal \| embryonic stage \| recessive (Gertler et al., 1995) lethal \| recessive (Ahern-Djamali et al., 1998, Comer et al., 1998) neuroanatomy defective (with ena^GC5) (Wills et al., 2002) neuroanatomy defective \| embryonic stage (with ena²³) (Gates et al., 2007) neuroanatomy defective \| embryonic stage (with ena²¹⁰) (Gates et al., 2007) neuroanatomy defective \| embryonic stage (with ena^GC5) (Song et al., 2010)
Phenotype Manifest In
	axon (Gertler et al., 1995) central nervous system (with ena²¹⁰) (Bashaw et al., 2000) commissure (Gertler et al., 1995) commissure (with ena²¹⁰) (Bashaw et al., 2000) embryonic/first instar larval cuticle (with ena^GC5) (Gates et al., 2007) embryonic dorsal epidermis (with ena^GC5) (Gates et al., 2007) filopodium (Gonçalves-Pimentel et al., 2011) filopodium (with ena²³) (Gonçalves-Pimentel et al., 2011) intersegmental nerve (Wills et al., 1999) intersegmental nerve branch ISNb of A1-7 (with ena^GC5) (Song et al., 2010) longitudinal connective (Gertler et al., 1995) longitudinal connective (with ena²³) (Gates et al., 2007) longitudinal connective (with ena²¹⁰) (Gates et al., 2007) longitudinal connective (with ena^GC5) (Fan et al., 2003) peripheral nervous system (Gertler et al., 1995) presumptive embryonic/larval central nervous system (with ena^GC5) (Wills et al., 2002) stage 14 embryo (with ena²¹⁰) (Grevengoed et al., 2001)
Detailed Description
	Statement Reference Cultured primary neurons derived from ena[GC1] and ena[GC1]/ena[23] 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) ena[23]/ena[GC1] and ena[210]/ena[GC1] embryos have reduced longitudinal axons in the central nervous system. Embryos that are both maternally and zygotically mutant for ena (ena[23]/ena[GC1] embryos derived from females with homozygous ena[23] 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[23]/ena[GC1] embryos derived from females with homozygous ena[23] 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[210]/ena[GC1] embryos derived from females with homozygous ena[210] 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) 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 the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Suppressed by
Statement Reference ena^GC5/ena^GC1 has lethal phenotype, suppressible \| partially by Hsap\VASP^{Scer\UAS.cADa}/Scer\GAL4^e22c (Ahern-Djamali et al., 1998)
NOT suppressed by
Statement Reference ena^GC5/ena^GC1 has neuroanatomy defective \| embryonic stage phenotype, non-suppressible by Dab¹/Dab[+] (Song et al., 2010)
Suppressor of
Statement Reference ena[+]/ena^GC1 is a suppressor \| partially of neuroanatomy defective \| maternal effect \| embryonic stage phenotype of Dab²/Dab¹ (Song et al., 2010) ena[+]/ena^GC1 is a suppressor of neuroanatomy defective phenotype of DAAM^{C.Scer\UAS.P\T} (Matusek et al., 2008)
Other
Statement Reference Hsap\VASP^{Scer\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 central nervous system phenotype, enhanceable by robo[+]/robo⁴ (Bashaw et al., 2000) ena^GC1/ena²¹⁰ has commissure phenotype, enhanceable by robo[+]/robo⁴ (Bashaw et al., 2000) ena^GC1/ena²¹⁰ has longitudinal connective phenotype, enhanceable by robo[+]/robo⁴ (Bashaw et al., 2000) ena^GC1/ena²¹⁰ has pCC neuron phenotype, enhanceable by robo[+]/robo⁴ (Bashaw et al., 2000)
NOT suppressed by
Statement Reference ena^GC5/ena^GC1 has intersegmental nerve branch ISNb of A1-7 phenotype, non-suppressible by Dab¹/Dab[+] (Song et al., 2010)
Enhancer of
Statement Reference ena[+], ena^GC1, Scer\GAL4^GMR.PF is an enhancer of eye \| pupal stage phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, cindr^{dsRNA.Scer\UAS} (Johnson and Cagan, 2009) ena[+]/ena^GC1 is an enhancer of longitudinal connective phenotype of robo⁵, sli[+]/sli¹ (Bashaw et al., 2000) ena[+]/ena^GC1 is an enhancer of photoreceptor cell R7 & axon phenotype of Lar^5.5/Lar²¹²⁷ (Maurel-Zaffran et al., 2001) ena^GC1 is an enhancer of intersegmental nerve \| heat sensitive phenotype of N^l1N-ts1 (Crowner et al., 2003) robo[+], ena[+], ena^GC1, robo⁵ is an enhancer of longitudinal connective phenotype of sli¹ (Bashaw et al., 2000)
NOT Enhancer of
Statement Reference ena[+]/ena^GC1 is a non-enhancer of 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 intersegmental nerve branch ISNb of A1-7 \| maternal effect phenotype of Dab²/Dab¹ (Song et al., 2010) ena[+]/ena^GC1 is a suppressor of commissure \| embryonic stage phenotype of DAAM^{C.Scer\UAS.P\T}, Scer\GAL4^elav-C155 (Matusek et al., 2008) ena[+]/ena^GC1 is a suppressor of commissure phenotype of Scer\GAL4^unspecified, robo^Y-F.Scer\UAS (Bashaw et al., 2000) ena[+]/ena^GC1 is a suppressor of fascicle \| embryonic stage phenotype of DAAM^{C.Scer\UAS.P\T}, Scer\GAL4^elav-C155 (Matusek et al., 2008) ena^GC1 is a suppressor \| partially of ventral nerve cord commissure phenotype of Scer\GAL4^elav.PLu, lea^Scer\UAS.cSa (Simpson et al., 2000) ena^GC1 is a suppressor of commissure phenotype of comm¹ (Bashaw et al., 2000) ena^GC1 is a suppressor of commissure phenotype of Scer\GAL4^unspecified, fra::robo^{Scer\UAS.FR.T:Hsap\MYC} (Bashaw et al., 2000) ena^GC1 is a suppressor of commissure phenotype of Scer\GAL4^unspecified, lea^EP (Bashaw 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/Scer\GAL4^GMR.PF, Sema-1a^Scer\UAS.cYa (Yu et al., 2010) ena^GC1 is a non-suppressor of lamina \| third instar larval stage phenotype of Scer\GAL4^GMR.PF/Scer\GAL4^GMR.PF, Sema-1a^Scer\UAS.cYa (Yu et al., 2010)
Other
Statement Reference arm⁸, ena^GC1 has dorsal closure embryo phenotype (Grevengoed et al., 2001, Grevengoed et al., 2001) arm⁸, ena^GC1 has stage 14 embryo phenotype (Grevengoed et al., 2001, 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 Dab[1]/Dab[2] females and having Dab[1] 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[1]/+. (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.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 & Rescue Data
Fails to complement	ena^C14-06 (Sano et al., 2012)
Partially rescued by	ena^GC5/ena^GC1 is partially rescued by ena^{K636stop.Scer\UAS}/Scer\GAL4^e22c (Ahern-Djamali et al., 1998) ena^GC5/ena^GC1 is partially rescued by ena^Scer\UAS.cCa/Scer\GAL4^e22c (Comer et al., 1998) ena^GC5/ena^GC1 is partially rescued by ena^Scer\UAS.cCa/Scer\GAL4^neu (Wills et al., 1999) ena^GC5/ena^GC1 is partially rescued by Scer\GAL4^e22c/ena^{Scer\UAS.cADa} (Ahern-Djamali et al., 1998) ena^GC5/ena^GC1 is partially rescued by Scer\GAL4^e22c/ena^YF.Scer\UAS (Comer et al., 1998)
Comments
Stocks ( 1 )
Bloomington	8569 Adh^fn6 pr¹ cn¹ ena^GC1/CyO
Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym	ena^GC1 (Gates et al., 2007, Johnson and Cagan, 2009, Matusek et al., 2008, Song et al., 2010, Yu et al., 2010, Gonçalves-Pimentel et al., 2011, Sano et al., 2012) enb^GC1
Name Synonym
Secondary FlyBase IDs

References ( 19 )
Research paper	Sano et al., 2012, PLoS ONE 7(12): e52649 The Drosophila Actin Regulator ENABLED Regulates Cell Shape and Orientation during Gonad Morphogenesis. [FBrf0220491] Gonçalves-Pimentel et al., 2011, PLoS ONE 6(3): e18340 Dissecting regulatory networks of filopodia formation in a Drosophila growth cone model. [FBrf0213367] Song et al., 2010, Development 137(21): 3719--3727 Disabled is a bona fide component of the Abl signaling network. [FBrf0212092] Yu et al., 2010, J. Neurosci. 30(36): 12151--12156 Plexin a-semaphorin-1a reverse signaling regulates photoreceptor axon guidance in Drosophila. [FBrf0211784] Johnson and Cagan, 2009, PLoS ONE 4(9): e7008 A quantitative method to analyze Drosophila pupal eye patterning. [FBrf0208849] Matusek et al., 2008, J. Neurosci. 28(49): 13310--13319 Formin proteins of the DAAM subfamily play a role during axon growth. [FBrf0206320] Gates et al., 2007, Development 134(11): 2027--2039 Enabled plays key roles in embryonic epithelial morphogenesis in Drosophila. [FBrf0201861] Crowner et al., 2003, Curr. Biol. 13(11): 967--972 Notch Steers Drosophila ISNb Motor Axons by Regulating the Abl Signaling Pathway. [FBrf0159717] Fan et al., 2003, Neuron 40(1): 113--127 Slit stimulation recruits Dock and Pak to the roundabout receptor and increases Rac activity to regulate axon repulsion at the CNS midline. [FBrf0167957] Wills et al., 2002, Neuron 36(4): 611--622 A Drosophila homolog of cyclase-associated proteins collaborates with the abl tyrosine kinase to control midline axon pathfinding. [FBrf0152273] Grevengoed et al., 2001, J. Cell Biol. 155(7): 1185--1198 Abelson kinase regulates epithelial morphogenesis in Drosophila. [FBrf0141596] Maurel-Zaffran et al., 2001, Neuron 32(2): 225--235 Cell-autonomous and -nonautonomous functions of LAR in R7 photoreceptor axon targeting. [FBrf0139775] Shim et al., 2001, Development 128(23): 4923--4933 The Drosophila ribbon gene encodes a nuclear BTB domain protein that promotes epithelial migration and morphogenesis. [FBrf0141499] Bashaw et al., 2000, Cell 101(7): 703--715 Repulsive axon guidance: abelson and enabled play opposing roles downstream of the roundabout receptor. [FBrf0128391] Simpson et al., 2000, Neuron 28(3): 753--766 Short-range and long-range guidance by Slit and its Robo receptors: robo and Robo2 play distinct roles in midline guidance. [FBrf0132431] Wills et al., 1999, Neuron 22(2): 301--312 The tyrosine kinase Abl and its substrate enabled collaborate with the receptor phosphatase Dlar to control motor axon guidance. [FBrf0108074] Ahern-Djamali et al., 1998, Mol. Biol. Cell 9(8): 2157--2171 Mutations in Drosophila enabled and rescue by human vasodilator-stimulated phosphoprotein (VASP) indicate important functional roles for Ena/VASP homology domain 1 (EVH1) and EVH2 domains. [FBrf0104394] Comer et al., 1998, Mol. Cell. Biol. 18(1): 152--160 Phosphorylation of Enabled by the Drosophila Abelson tyrosine kinase regulates the in vivo function and protein-protein interactions of Enabled. [FBrf0099996] Gertler et al., 1995, Genes Dev. 9(5): 521--533 enabled, a dosage-sensitive suppressor of mutations in the Drosophila Abl tyrosine kinase, encodes an Abl substrate with SH3 domain-binding properties. [FBrf0080046]

Allele Dmel\enaGC1

Allele Dmel\ena^GC1