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General Information
Symbol
Dmel\ena23
Species
D. melanogaster
Name
FlyBase ID
FBal0093019
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Mutagen
    Nature of the Allele
    Allele class
    Mutagen
    Mutations Mapped to the Genome
     
    Type
    Location
    Additional Notes
    References
    point mutation
    Nucleotide change:
    A19161413T
    Reported nucleotide change:
    A?G
    Amino acid change:
    K636term | ena-PA; K785term | ena-PB; K636term | ena-PC; K639term | ena-PD; K636term | ena-PE; K932term | ena-PF; K616term | ena-PG
    Reported amino acid change:
    N379F
    Comment:
    An additional amino acid change at or near amino acid residue 379 is also observed in ena[23].
    Associated Sequence Data
    DNA sequence
    Protein sequence
     
     
    Progenitor genotype
    Cytology
    Nature of the lesion
    Statement
    Reference
    Nucleotide substitution: A?G.
    Nucleotide substitution: A?T.
    Amino acid replacement: N379F.
    Amino acid replacement: K636term.
    Expression Data
    Reporter Expression
    Additional Information
    Statement
    Reference
     
    Marker for
    Reflects expression of
    Reporter construct used in assay
    Human Disease Associations
    Disease Ontology (DO) Annotations
    Models Based on Experimental Evidence ( 0 )
    Disease
    Evidence
    References
    Modifiers Based on Experimental Evidence ( 0 )
    Disease
    Interaction
    References
    Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
     
    Phenotypic Data
    Phenotypic Class
    Phenotype Manifest In
    Detailed Description
    Statement
    Reference
    ena23 zygotic/maternal mutant embryos display a wavy leading edge during dorsal closure, with defects in leading edge cell shape, a reduced rate of zippering and deep and persistent segmental grooves. Approximately 90% of ena23 zygotic mutants exhibit virtually wild-type cuticles, whereas 8% display head holes.
    Cultured primary neurons derived from ena23 and enaGC1/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.
    24% of eggs derived from females carrying homozygous germline clones show a "dumpless" phenotype. Egg chambers in females with homozygous germline clones have defects in the cytoplasmic filaments (the bundled cytoplasmic actin filaments extending from the cortex to nuclei). No defects in ring canal formation or growth are seen in mutant egg chambers. Some egg chambers contain multinucleate nurse cells. Homozygous follicle cell clones do not usually cause significant disruptions in either epithelial organisation or in the assembly of cortical actin into follicle cells adherens junctions in stage 2-7 egg chambers. However, in later egg chambers, clones with reduced cortical actin and disruptions in epithelial integrity are seen.
    Leading edge cells in embryos that are maternally and zygotically mutant for ena show a large decrease in average lamellipodial area and a striking decrease in filopodial number.
    Homozygous clones that encompass the morphogenetic furrow do not result in a defect in cell constriction in the morphogenetic furrow.
    ena23/enaGC1 embryos have reduced longitudinal axons in the central nervous system. 74% of zygotic ena23 mutant embryos have a wild-type cuticle, while 21% show misalignment/puckering along the dorsal midline. Mature 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.
    Single cell γ neuron mutant clones in the mushroom body show drastic axon growth defects.
    Homozygous embryos do not show midline crossing errors by axons in the central nervous system.
    Mutant follicle cell clones lose cortical actin filaments from apical, basal and lateral sites.
    96% of ISNb axons show a bypass phenotype in homozygous embryos.
    Lethal in combination with enaGC1.
    External Data
    Interactions
    Show genetic interaction network for Enhancers & Suppressors
    Phenotypic Class
    Enhanced by
    Statement
    Reference
    ena23 has cell shape defective phenotype, enhanceable by pyd[+]/pydB12
    ena23 has cell shape defective phenotype, enhanceable by pydex180/pyd[+]
    ena23 has cell shape defective phenotype, enhanceable by cnoR2/cno[+]
    Enhancer of
    Statement
    Reference
    ena23/ena[+] is an enhancer of cell shape defective phenotype of cnoR2
    ena23/ena[+] is an enhancer of visible phenotype of fjN7
    Suppressor of
    NOT Suppressor of
    Statement
    Reference
    ena23/ena[+] is a non-suppressor of neuroanatomy defective | semidominant | embryonic stage phenotype of mir-8Δ
    Other
    Statement
    Reference
    Phenotype Manifest In
    Enhanced by
    Statement
    Reference
    ena23 has embryo | dorsal closure stage phenotype, enhanceable by pyd[+]/pydB12
    ena23 has embryonic leading edge cell phenotype, enhanceable by pyd[+]/pydB12
    ena23 has ventral head epidermis phenotype, enhanceable by pyd[+]/pydB12
    ena23 has embryonic head phenotype, enhanceable by pyd[+]/pydB12
    ena23 has embryo | dorsal closure stage phenotype, enhanceable by pydex180/pyd[+]
    ena23 has embryonic leading edge cell phenotype, enhanceable by pydex180/pyd[+]
    ena23 has ventral head epidermis phenotype, enhanceable by pydex180/pyd[+]
    ena23 has embryonic head phenotype, enhanceable by pydex180/pyd[+]
    ena23 has embryo | dorsal closure stage phenotype, enhanceable by cnoR2/cno[+]
    ena23 has embryonic leading edge cell phenotype, enhanceable by cnoR2/cno[+]
    ena23 has ventral head epidermis phenotype, enhanceable by cnoR2/cno[+]
    ena23 has embryonic head phenotype, enhanceable by cnoR2/cno[+]
    Enhancer of
    Statement
    Reference
    ena23/ena[+] is an enhancer of embryo | dorsal closure stage phenotype of cnoR2
    ena23/ena[+] is an enhancer of embryonic leading edge cell phenotype of cnoR2
    ena23/ena[+] is an enhancer of ventral head epidermis phenotype of cnoR2
    ena23/ena[+] is an enhancer of embryonic head phenotype of cnoR2
    ena23/ena[+] is an enhancer of embryo | dorsal closure stage phenotype of pydB12
    ena23/ena[+] is an enhancer of embryonic leading edge cell phenotype of pydB12
    ena23/ena[+] is an enhancer of ventral head epidermis phenotype of pydB12
    ena23/ena[+] is an enhancer of embryonic head phenotype of pydB12
    ena23/ena[+] is an enhancer of embryo | dorsal closure stage phenotype of pydex180
    ena23/ena[+] is an enhancer of embryonic leading edge cell phenotype of pydex180
    ena23/ena[+] is an enhancer of ventral head epidermis phenotype of pydex180
    ena23/ena[+] is an enhancer of embryonic head phenotype of pydex180
    ena23/ena[+] is an enhancer of joint phenotype of fjN7
    Suppressor of
    NOT Suppressor of
    Statement
    Reference
    ena23/ena[+] is a non-suppressor of axon | embryonic stage phenotype of mir-8Δ
    Other
    Additional Comments
    Genetic Interactions
    Statement
    Reference
    ena23/+ does not rescue the neuromuscular junction formation phenotype (intersegmental nerve branch ISNb motor axon innervation defects at m6/7) seen in mir-8Δ/+ embryos.
    An ena23 heterozygous mutant background suppresses the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing CskGD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4ptc-559.1. An ena23/+ background suppresses the cell migration seen upon expression of Rho1Scer\UAS.cMa under the control of Scer\GAL4ptc-559.1. An ena23/+ background suppresses the cell migration seen upon expression of hepScer\UAS.cUa under the control of Scer\GAL4ptc-559.1.
    ena23 is unable to suppress the fertility defects seen in Df(1)NetABΔ. The courtship behaviour defects seen in Df(1)NetABΔ mutant males are also not rescued.
    Reducing pyd levels, through a pydB12 or pydex180 heterozygous background, strongly enhances the morphogenesis defects found in zygotic ena23 mutants, substantially increasing the frequency of failure of head involution. Reducing ena levels, through an ena23 heterozygous background, substantially enhances the severity of the pydB12 or pydex180 zygotic/maternal phenotype; more than one-third of the mutants exhibit large holes in the cuticle, suggesting disruption of epithelial integrity. An ena23 heterozygous background enhances the cnoR2 zygotic phenotype, with 38% of progeny exhibiting head and/or dorsal holes, and 4% displaying a novel, stronger phenotype in which only the ventral cuticle remains. Reducing maternal and zygotic cnoR2 levels strongly enhances the ena23 zygotic phenotype, with 50% of the progeny exhibiting head holes. cnoR2 ena23 double mutants fail to complete dorsal closure.
    Cultured primary neurons derived from ena23/+ Sop21/+ and DAAMEx68/+ ena23/+ double heterozygous embryos show a significant reduction in the number of filopodia compared to control neurons. Cultured primary neurons derived from chic221/+ ena23/+ and chic05205a/+ ena23/+ double heterozygous embryos show a significant reduction in the number of filopodia compared to control neurons.
    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 ena23/+ background.
    Xenogenetic Interactions
    Statement
    Reference
    Complementation and Rescue Data
    Comments
    Images (0)
    Mutant
    Wild-type
    Stocks (2)
    Notes on Origin
    Discoverer
    External Crossreferences and Linkouts ( 0 )
    Synonyms and Secondary IDs (3)
    References (21)