Allele Dmel\ena²¹⁰

General Information
Symbol	Dmel\ena²¹⁰	Species	D. melanogaster
Name		FlyBase ID	FBal0031206
Feature type	allele	Created / Updated	2006-08-22/2006-08-22
Associated gene	Dmel\ena

Allele class
Mutagen
Nature of the Allele
Allele class
Mutagen
Mapped Features and Mutations
Type Symbol & 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 Amino acid replacement: A97V. Nucleotide substitution: C to T. (Ahern-Djamali et al., 1998)
Assay mode
Cytology
Phenotypic Data
Phenotypic Class
	lethal \| recessive (Ahern-Djamali et al., 1998) lethal \| embryonic stage \| recessive (Gertler et al., 1995) neuroanatomy defective \| somatic clone (Ng and Luo, 2004)
Phenotype Manifest In
	central nervous system (with ena^GC1) (Bashaw et al., 2000) commissure (with ena^GC1) (Bashaw et al., 2000) stage 14 embryo (with ena^GC1) (Grevengoed et al., 2001) anterior fascicle (Wills et al., 1999) adult mushroom body \| somatic clone (Ng and Luo, 2004)
Detailed Description
	Statement Reference CNS and PNS defects. (Gertler et al., 1995) Lethal in combination with ena^GC1. (Ahern-Djamali et al., 1998) 79% of ISNb axons show a bypass phenotype in homozygous embryos. (Wills et al., 1999) 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) Most ena^GC1/ena²¹⁰ embryos only have mild defects in head involution. (Grevengoed et al., 2001) Single cell γ neuron mutant clones in the mushroom body show drastic axon growth defects. (Ng and Luo, 2004)
Interactions
	Show the genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement Reference ena[+]/ena²¹⁰ is an enhancer of visible phenotype of fj^N7 (Buckles et al., 2001)
Suppressor of
Statement Reference ena[+]/ena²¹⁰ is a suppressor of neuroanatomy defective phenotype of Abl⁴ (Wills et al., 2002) ena[+]/ena²¹⁰ is a suppressor of mitotic cell cycle defective \| maternal effect phenotype of Abl⁴ (Grevengoed et al., 2003) ena[+]/ena²¹⁰ is a suppressor of lethal phenotype of Abl^unspecified (Gertler et al., 1990) ena[+]/ena²¹⁰ is a suppressor of lethal phenotype of Abl^unspecified, Nrt^unspecified (Gertler et al., 1990)
Phenotype Manifest In
Enhanced by
Statement Reference 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) ena^GC1/ena²¹⁰ has central nervous system phenotype, enhanceable by robo[+]/robo⁴ (Bashaw et al., 2000)
Enhancer of
Statement Reference ena[+]/ena²¹⁰ is an enhancer of joint phenotype of fj^N7 (Buckles et al., 2001)
Suppressor of
Statement Reference ena[+]/ena²¹⁰ is a suppressor of embryonic central nervous system phenotype of Abl⁴ (Wills et al., 2002)
Other
Statement Reference arm⁴, ena²¹⁰ has embryonic/first instar larval cuticle \| dorsal phenotype (Grevengoed et al., 2001, Grevengoed et al., 2001)
Additional Comments
Genetic Interactions
Statement Reference In Abl mutant embryos the ena²¹⁰ mutation acts in a dominant fashion and allows a high recovery of fertile adults. Rescue also acts on Abl and Nrt double mutants. Nrt mutant individuals with the ena²¹⁰ mutation survive to adult stages. (Gertler et al., 1990) 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) The midline crossing errors seen in the central nervous system of Abl⁴/Abl⁴ embryos are suppressed by ena²¹⁰/+. (Wills et al., 2002) The dorsal side of arm⁴/Y ; ena²¹⁰/ena²¹⁰ embryos is completely open. (Grevengoed et al., 2001) ena²¹⁰ heterozygosity strongly suppresses the cellularisation phenotype of Abl⁴ mutants. The majority of suppressed embryos exhibit far fewer multinucleate cells and less apical actin. (Grevengoed et al., 2003)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Fails to complement	ena⁴⁶ (Gao et al., 1999)
Rescued by	ena²¹⁰ is rescued by ena^8PA (Ahern-Djamali et al., 1999) ena²¹⁰ is rescued by ena^tAa (Ahern-Djamali et al., 1999)
Comments
Stocks ( 1 )
Bloomington	8568 wg^Sp-1 Bl¹ ena²¹⁰/CyO
Notes on Origin
Discoverer

Synonyms & Secondary IDs ( 3 )
Reported As
Symbol Synonym	ena²¹⁰ enb^2.10 (Bennett and Hoffmann, 1992) enb²¹⁰
Name Synonym
Secondary FlyBase IDs

References ( 17 )
Research paper	Forsthoefel et al., 2005, Development 132(8): 1983--1994 The Abelson tyrosine kinase, the Trio GEF and Enabled interact with the Netrin receptor Frazzled in Drosophila. [FBrf0183931] Ng and Luo, 2004, Neuron 44(5): 779--793 Rho GTPases Regulate Axon Growth through Convergent and Divergent Signaling Pathways. [FBrf0180582] Grevengoed et al., 2003, J. Cell Biol. 163(6): 1267--1279 Balancing different types of actin polymerization at distinct sites: roles for Abelson kinase and Enabled. [FBrf0167770] 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] Baum and Perrimon, 2001, Nature Cell Biol. 3(10): 883--890 Spatial control of the actin cytoskeleton in Drosophila epithelial cells. [FBrf0139770] Buckles et al., 2001, Development 128(18): 3533--3542 four-jointed interacts with dachs, abelson and enabled and feeds back onto the Notch pathway to affect growth and segmentation in the Drosophila leg. [FBrf0138378] Grevengoed et al., 2001, J. Cell Biol. 155(7): 1185--1198 Abelson kinase regulates epithelial morphogenesis in Drosophila. [FBrf0141596] Bashaw et al., 2000, Cell 101(7): 703--715 Repulsive axon guidance: abelson and enabled play opposing roles downstream of the roundabout receptor. [FBrf0128391] Ahern-Djamali et al., 1999, Proc. Natl. Acad. Sci. USA 96(9): 4977--4982 Identification of profilin and src homology 3 domains as binding partners for Drosophila enabled. [FBrf0108135] Gao et al., 1999, Genes Dev. 13(19): 2549--2561 Genes regulating dendritic outgrowth, branching, and routing in Drosophila. [FBrf0111874] 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, Molec. 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] Saha and Sinha, 1996, J. Genet. 75(2): 161--172 Genetic interaction of Drosophila homologue of abelson (abl) proto-oncogene (D-abl) and lethal (2) giant larvae (lgl) tumour suppressor gene during embryonic development. [FBrf0093687] 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] Bennett and Hoffmann, 1992, Development 116(4): 953--966 Increased levels of the Drosophila Abelson tyrosine kinase in nerves and muscles: subcellular localization and mutant phenotypes imply a role in cell-cell interactions. [FBrf0055913] Gertler et al., 1990, Science 248: 857--860 Genetic suppression of mutations in the Drosophila abl proto-oncogene homolog. [FBrf0052941]
Abstract	Siegrist et al., 1999, A. Dros. Res. Conf. 40: 296A Directing Actin Assembly through a Zyxin and Enabled (Ena) Connection. [FBrf0107264]

Allele Dmel\ena210

Allele Dmel\ena²¹⁰