FlyBase Allele Report: Dmel\ena[23]

General Information

Symbol

Dmel\ena²³

Species

D. melanogaster

Name

FlyBase ID

FBal0093019

Feature type

allele

Associated gene

Dmel\ena

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

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Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

Mutations Mapped to the Genome

Type

Location

Additional Notes

References

point_mutation

2R:19,161,413..19,161,413 [+]

Nucleotide change:

A19161413T

Reported nucleotide change:

A?G

Amino acid change:

Reported amino acid change:

N379F

Comment:

An additional amino acid change at or near amino acid residue 379 is also observed in ena[23].

(Ahern-Djamali et al., 1998)

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

Progenitor genotype

Cytology

Nature of the lesion

Statement

Reference

Nucleotide substitution: A?G.

(Ahern-Djamali et al., 1998)

Nucleotide substitution: A?T.

(Ahern-Djamali et al., 1998)

Amino acid replacement: N379F.

(Ahern-Djamali et al., 1998)

Amino acid replacement: K636term.

(Ahern-Djamali et al., 1998)

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 ( 1 )

Disease

Interaction

References

ameliorates chronic myeloid leukemia

modeled by Hsap\ABL1::Hsap\BCR^UAS.cBa

(Bernardoni et al., 2019)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

actin filament & egg chamber | germ-line clone

(Gates et al., 2009)

adult mushroom body | somatic clone

(Ng and Luo, 2004)

adult mushroom body gamma-lobe | somatic clone

(Yaniv et al., 2020)

axon | adult stage | somatic clone

(Yaniv et al., 2020)

egg | germline clone | maternal effect

(Gates et al., 2009)

embryo | dorsal closure stage

(Choi et al., 2011)

embryonic/first instar larval cuticle

(Gates et al., 2007)

embryonic/first instar larval cuticle | maternal effect

(Gates et al., 2007)

embryonic dorsal epidermis

(Gates et al., 2007)

embryonic head

(Choi et al., 2011)

embryonic head | maternal effect

(Gates et al., 2007)

embryonic head epidermis | maternal effect

(Gates et al., 2007)

embryonic leading edge cell

(Choi et al., 2011)

filopodium

(Gonçalves-Pimentel et al., 2011, Homem and Peifer, 2009)

filopodium (with ena^GC1)

(Gonçalves-Pimentel et al., 2011)

follicle cell & actin filament | somatic clone

(Baum and Perrimon, 2001)

lamellipodium

(Homem and Peifer, 2009)

larval intersegmental nerve

(Wills et al., 1999)

larval longitudinal connective (with ena^GC1)

(Gates et al., 2007)

ventral head epidermis

(Choi et al., 2011)

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.

(Choi et al., 2011)

Cultured primary neurons derived from ena²³ 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)

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.

(Gates et al., 2009)

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.

(Homem and Peifer, 2009)

Homozygous clones that encompass the morphogenetic furrow do not result in a defect in cell constriction in the morphogenetic furrow.

(Corrigall et al., 2007)

ena²³/ena^GC1 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/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.

(Gates et al., 2007)

Single cell γ neuron mutant clones in the mushroom body show drastic axon growth defects.

(Ng and Luo, 2004)

Homozygous embryos do not show midline crossing errors by axons in the central nervous system.

(Wills et al., 2002)

Mutant follicle cell clones lose cortical actin filaments from apical, basal and lateral sites.

(Baum and Perrimon, 2001)

96% of ISNb axons show a bypass phenotype in homozygous embryos.

(Wills et al., 1999)

Lethal in combination with ena^GC1.

(Ahern-Djamali et al., 1998)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

ena²³ has abnormal cell shape phenotype, enhanceable by pyd[+]/pyd^B12

(Choi et al., 2011)

ena²³ has abnormal cell shape phenotype, enhanceable by pyd^ex180/pyd[+]

(Choi et al., 2011)

ena²³ has abnormal cell shape phenotype, enhanceable by cno^R2/cno[+]

(Choi et al., 2011)

Enhancer of

Statement

Reference

ena²³/ena[+] is an enhancer of abnormal cell shape phenotype of cno^R2

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of visible phenotype of fj^N7

(Buckles et al., 2001)

Suppressor of

Statement

Reference

ena²³/ena[+] is a suppressor of visible | adult stage phenotype of Hsap\ABL1::Hsap\BCR^UAS.cBa, Scer\GAL4^GMR.PU

(Bernardoni et al., 2019)

ena²³/ena[+] is a suppressor of abnormal cell migration phenotype of Csk^GD9345, Scer\GAL4^ptc-559.1

(Rudrapatna et al., 2014)

ena²³/ena[+] is a suppressor of abnormal cell migration phenotype of Rho1^UAS.cMa, Scer\GAL4^ptc-559.1

(Rudrapatna et al., 2014)

ena²³/ena[+] is a suppressor of abnormal cell migration phenotype of Scer\GAL4^ptc-559.1, hep^UAS.cUa

(Rudrapatna et al., 2014)

ena²³/ena[+] is a suppressor of abnormal neuroanatomy phenotype of DAAM^C.UASp/DAAM^{C.Scer\UAS.P\T}

(Matusek et al., 2008)

NOT Suppressor of

Statement

Reference

ena²³/ena[+] is a non-suppressor of abnormal neuroanatomy | semidominant | embryonic stage phenotype of mir-8^Δ

(Lu et al., 2014)

Other

Statement

Reference

Csk^GD9345, ena²³ has lethal phenotype

(Rudrapatna et al., 2014)

Phenotype Manifest In

Enhanced by

Statement

Reference

ena²³ has embryo | dorsal closure stage phenotype, enhanceable by pyd[+]/pyd^B12

(Choi et al., 2011)

ena²³ has embryonic leading edge cell phenotype, enhanceable by pyd[+]/pyd^B12

(Choi et al., 2011)

ena²³ has ventral head epidermis phenotype, enhanceable by pyd[+]/pyd^B12

(Choi et al., 2011)

ena²³ has embryonic head phenotype, enhanceable by pyd[+]/pyd^B12

(Choi et al., 2011)

ena²³ has embryo | dorsal closure stage phenotype, enhanceable by pyd^ex180/pyd[+]

(Choi et al., 2011)

ena²³ has embryonic leading edge cell phenotype, enhanceable by pyd^ex180/pyd[+]

(Choi et al., 2011)

ena²³ has ventral head epidermis phenotype, enhanceable by pyd^ex180/pyd[+]

(Choi et al., 2011)

ena²³ has embryonic head phenotype, enhanceable by pyd^ex180/pyd[+]

(Choi et al., 2011)

ena²³ has embryo | dorsal closure stage phenotype, enhanceable by cno^R2/cno[+]

(Choi et al., 2011)

ena²³ has embryonic leading edge cell phenotype, enhanceable by cno^R2/cno[+]

(Choi et al., 2011)

ena²³ has ventral head epidermis phenotype, enhanceable by cno^R2/cno[+]

(Choi et al., 2011)

ena²³ has embryonic head phenotype, enhanceable by cno^R2/cno[+]

(Choi et al., 2011)

Suppressed by

Statement

Reference

Atg9^B5, ena²³ has nurse cell phenotype, suppressible by Atg9^Tag:HA

(Kiss et al., 2020)

Enhancer of

Statement

Reference

ena²³/ena[+] is an enhancer of nurse cell phenotype of Atg9^B5

(Kiss et al., 2020)

ena²³, chic[+], ena[+], chic²²¹ is an enhancer of nurse cell phenotype of Atg9^B5

(Kiss et al., 2020)

ena²³/ena[+] is an enhancer of embryo | dorsal closure stage phenotype of cno^R2

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of embryonic leading edge cell phenotype of cno^R2

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of ventral head epidermis phenotype of cno^R2

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of embryonic head phenotype of cno^R2

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of embryo | dorsal closure stage phenotype of pyd^B12

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of embryonic leading edge cell phenotype of pyd^B12

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of ventral head epidermis phenotype of pyd^B12

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of embryonic head phenotype of pyd^B12

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of embryo | dorsal closure stage phenotype of pyd^ex180

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of embryonic leading edge cell phenotype of pyd^ex180

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of ventral head epidermis phenotype of pyd^ex180

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of embryonic head phenotype of pyd^ex180

(Choi et al., 2011)

ena²³/ena[+] is an enhancer of leg joint phenotype of fj^N7

(Buckles et al., 2001)

Suppressor of

Statement

Reference

ena²³/ena[+] is a suppressor of eye phenotype of Hsap\ABL1::Hsap\BCR^UAS.cBa, Scer\GAL4^GMR.PU

(Bernardoni et al., 2019)

ena²³/ena[+] is a suppressor of wing disc phenotype of Csk^GD9345, Scer\GAL4^ptc-559.1

(Rudrapatna et al., 2014)

ena²³/ena[+] is a suppressor of wing disc phenotype of Rho1^UAS.cMa, Scer\GAL4^ptc-559.1

(Rudrapatna et al., 2014)

ena²³/ena[+] is a suppressor of wing disc phenotype of Scer\GAL4^ptc-559.1, hep^UAS.cUa

(Rudrapatna et al., 2014)

ena²³/ena[+] is a suppressor of neuropil | embryonic stage phenotype of DAAM^C.UASp/DAAM^{C.Scer\UAS.P\T}, Scer\GAL4^elav-C155

(Matusek et al., 2008)

ena²³/ena[+] is a suppressor of fascicle | embryonic stage phenotype of DAAM^C.UASp/DAAM^{C.Scer\UAS.P\T}, Scer\GAL4^elav-C155

(Matusek et al., 2008)

ena²³/ena[+] is a suppressor of symmetrical commissure | embryonic stage phenotype of DAAM^C.UASp/DAAM^{C.Scer\UAS.P\T}, Scer\GAL4^elav-C155

(Matusek et al., 2008)

NOT Suppressor of

Statement

Reference

ena²³/ena[+] is a non-suppressor of larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype of mir-8^Δ

(Lu et al., 2014)

ena²³/ena[+] is a non-suppressor of axon | embryonic stage phenotype of mir-8^Δ

(Lu et al., 2014)

Other

Statement

Reference

Atg9^B5, chic[+]/chic²²¹, ena²³/ena[+] has nurse cell ring canal | decreased number phenotype

(Kiss et al., 2020)

Arpc1¹, ena²³/ena[+] has filopodium phenotype

(Gonçalves-Pimentel et al., 2011)

chic²²¹, ena²³/ena[+] has filopodium phenotype

(Gonçalves-Pimentel et al., 2011)

chic^05205a, ena²³/ena[+] has filopodium phenotype

(Gonçalves-Pimentel et al., 2011)

DAAM^Ex68, ena²³/ena[+] has filopodium phenotype

(Gonçalves-Pimentel et al., 2011)

Additional Comments

Genetic Interactions

Statement

Reference

chic²²¹/+ ena²³/+ in Atg9^B5background leads to a decrease in the number of ring canals in stage 9+ egg chambers.

(Kiss et al., 2020)

ena²³/+ does not rescue the neuromuscular junction formation phenotype (intersegmental nerve branch ISNb motor axon innervation defects at m6/7) seen in mir-8^Δ/+ embryos.

(Lu et al., 2014)

An ena²³ heterozygous mutant background suppresses the actin remodelling and subsequent basolateral invasion of epithelial cells seen in flies expressing Csk^GD9345 in a stripe of cells at the anterior/posterior boundary of the larval wing disc under the control of Scer\GAL4^ptc-559.1.

An ena²³/+ background suppresses the cell migration seen upon expression of Rho1^Scer\UAS.cMa under the control of Scer\GAL4^ptc-559.1.

An ena²³/+ background suppresses the cell migration seen upon expression of hep^Scer\UAS.cUa under the control of Scer\GAL4^ptc-559.1.

(Rudrapatna et al., 2014)

ena²³ is unable to suppress the fertility defects seen in Df(1)NetAB^Δ. The courtship behaviour defects seen in Df(1)NetAB^Δ mutant males are also not rescued.

(Newquist et al., 2013)

Reducing pyd levels, through a pyd^B12 or pyd^ex180 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 pyd^B12 or pyd^ex180 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 cno^R2 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 cno^R2 levels strongly enhances the ena²³ zygotic phenotype, with 50% of the progeny exhibiting head holes.

cno^R2 ena²³ double mutants fail to complete dorsal closure.

(Choi et al., 2011)

Cultured primary neurons derived from ena²³/+ Sop2¹/+ and DAAM^Ex68/+ 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 chic^05205a/+ ena²³/+ double heterozygous embryos show a significant reduction in the number of filopodia compared to control neurons.

(Gonçalves-Pimentel et al., 2011)

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 ena²³/+ background.

(Matusek et al., 2008)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

ena^C14-06

(Sano et al., 2012)

ena⁴⁶

(Gao et al., 1999)

Comments

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

8571

ena²³/CyO, P{act-lacZ.B}CB1

25405

w^*; P{FRT(w^hs)}G13 ena²³/CyO

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

ena²³

(Hildebrand et al., 2021, King et al., 2021, Cheong et al., 2020, Kiss et al., 2020, Yaniv et al., 2020, Bernardoni et al., 2019, Qu et al., 2017, Becker et al., 2016, Lu et al., 2014, Rudrapatna et al., 2014, Newquist et al., 2013, Sano et al., 2012, Choi et al., 2011, Gonçalves-Pimentel et al., 2011, Gates et al., 2009, Homem and Peifer, 2009, Matusek et al., 2008, Corrigall et al., 2007, Gates et al., 2007)

enb²³

Name Synonyms

enabled

(Newquist et al., 2013)

Secondary FlyBase IDs

References (27)

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