FlyBase Allele Report: Dmel\ena[210]

General Information

Symbol

Dmel\ena²¹⁰

Species

D. melanogaster

Name

FlyBase ID

FBal0031206

Feature type

allele

Associated gene

Dmel\ena

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

Progenitor genotype

Cytology

Description

Amino acid replacement: A97V. Nucleotide substitution: C to T.

(Ahern-Djamali et al., 1998)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2R:19,159,018..19,159,018 [+]

Nucleotide change:

C19159018T

Reported nucleotide change:

C?T

Amino acid change:

Reported amino acid change:

A97V

(Ahern-Djamali et al., 1998)

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

exacerbates tauopathy

modeled by Hsap\MAPT^UAS.cWa

(Feuillette et al., 2020)

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)

central nervous system (with ena^GC1)

(Bashaw et al., 2000)

dendrite | larval stage

(Stürner et al., 2022)

dendritic branch | decreased number | larval stage | somatic clone

(Stürner et al., 2022)

embryo | embryonic stage 14 (with ena^GC1)

(Grevengoed et al., 2001)

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 epidermis | maternal effect

(Gates et al., 2007)

larval intersegmental nerve

(Wills et al., 1999)

larval longitudinal connective (with ena^GC1)

(Gates et al., 2007)

larval multidendritic class III neuron | somatic clone

(Stürner et al., 2022)

symmetrical commissure (with ena^GC1)

(Bashaw et al., 2000)

Detailed Description

Statement

Reference

4% 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.

(Gates et al., 2009)

No neuromuscular junction defects are detectable in ena²¹⁰/+ larvae.

(Loya et al., 2009)

Wings from ena²¹⁰ heterozygotes resemble wildtype wings.

(Lyulcheva et al., 2008)

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

78% of zygotic ena²¹⁰ mutant embryos have a wild-type cuticle, while 17% show misalignment/puckering along the dorsal midline.

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.

(Gates et al., 2007)

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

(Ng and Luo, 2004)

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)

79% 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)

CNS and PNS defects.

(Gertler et al., 1995)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhancer of

Statement

Reference

ena[+]/ena²¹⁰ is an enhancer of visible | adult stage phenotype of Hsap\MAPT^UAS.cWa, Scer\GAL4^GMR.PF

(Feuillette et al., 2020)

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 abnormal cell migration phenotype of Csk^GD9345, Scer\GAL4^ptc-559.1

(Rudrapatna et al., 2014)

ena[+]/ena²¹⁰ is a suppressor of abnormal cell migration phenotype of Rho1^UAS.cMa, Scer\GAL4^ptc-559.1

(Rudrapatna et al., 2014)

ena[+]/ena²¹⁰ is a suppressor of abnormal cell migration phenotype of Scer\GAL4^ptc-559.1, hep^UAS.cUa

(Rudrapatna et al., 2014)

ena²¹⁰ is a suppressor of abnormal cell migration phenotype of hpo^42-47

(Lucas et al., 2013)

ena[+]/ena²¹⁰ is a suppressor | partially of abnormal neuroanatomy phenotype of mir-8^Δ2

(Loya et al., 2009)

ena[+]/ena²¹⁰ is a suppressor of paralytic | dominant | larval stage phenotype of Abl¹/Abl[+], Khc¹⁶

(Martin et al., 2005)

ena[+]/ena²¹⁰ is a suppressor of abnormal neuroanatomy | dominant | larval stage phenotype of Abl¹/Abl[+], Khc¹⁶

(Martin et al., 2005)

ena[+]/ena²¹⁰ is a suppressor of abnormal mitotic cell cycle | maternal effect phenotype of Abl⁴

(Grevengoed et al., 2003)

ena[+]/ena²¹⁰ is a suppressor of abnormal neuroanatomy phenotype of Abl⁴

(Wills et al., 2002)

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)

NOT Suppressor of

Statement

Reference

ena[+]/ena²¹⁰ is a non-suppressor of abnormal neuroanatomy | semidominant | embryonic stage phenotype of mir-8^Δ

(Lu et al., 2014)

Other

Statement

Reference

Csk^GD9345, ena²¹⁰ has lethal phenotype

(Rudrapatna et al., 2014)

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)

Enhancer of

Statement

Reference

ena[+]/ena²¹⁰ is an enhancer of eye phenotype of Hsap\MAPT^UAS.cWa, Scer\GAL4^GMR.PF

(Feuillette et al., 2020)

ena[+]/ena²¹⁰ is an enhancer of leg joint phenotype of fj^N7

(Buckles et al., 2001)

Suppressor of

Statement

Reference

ena[+]/ena²¹⁰ is a suppressor of wing disc phenotype of Csk^GD9345, Scer\GAL4^ptc-559.1

(Rudrapatna et al., 2014)

ena[+]/ena²¹⁰ is a suppressor of wing disc phenotype of Rho1^UAS.cMa, Scer\GAL4^ptc-559.1

(Rudrapatna et al., 2014)

ena[+]/ena²¹⁰ is a suppressor of wing disc phenotype of Scer\GAL4^ptc-559.1, hep^UAS.cUa

(Rudrapatna et al., 2014)

ena²¹⁰ is a suppressor of border follicle cell phenotype of hpo^42-47

(Lucas et al., 2013)

ena[+]/ena²¹⁰ is a suppressor | partially of embryonic/larval neuromuscular junction | third instar larval stage phenotype of mir-8^Δ2

(Loya et al., 2009)

ena[+]/ena²¹⁰ is a suppressor | partially of NMJ bouton | larval stage phenotype of mir-8^Δ2

(Loya et al., 2009)

ena[+]/ena²¹⁰ is a suppressor of wing phenotype of Scer\GAL4^Bx-MS1096, pico^{UAS.Tag:polyHis,Tag:MYC}

(Lyulcheva et al., 2008)

ena[+]/ena²¹⁰ is a suppressor of axon phenotype of Abl¹/Abl[+], Khc¹⁶

(Martin et al., 2005)

ena[+]/ena²¹⁰ is a suppressor of presumptive embryonic/larval central nervous system phenotype of Abl⁴

(Wills et al., 2002)

NOT Suppressor of

Statement

Reference

ena[+]/ena²¹⁰ is a non-suppressor of larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype of mir-8^Δ

(Lu et al., 2014)

ena[+]/ena²¹⁰ is a non-suppressor of axon | embryonic stage phenotype of mir-8^Δ

(Lu et al., 2014)

Other

Statement

Reference

arm⁴, ena²¹⁰ has embryonic/first instar larval cuticle | dorsal phenotype

(Grevengoed et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

ena²¹⁰/+ 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 ena²¹⁰ 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 ena²¹⁰/+ background suppresses the cell migration seen upon expression of Rho1^Scer\UAS.cMa under the control of Scer\GAL4^ptc-559.1.

An ena²¹⁰/+ 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)

The border cell migration phenotype found in hpo^42-47 mutants is suppressed by a ena²¹⁰ background. These double mutants exhibit a normally polarised actin cytoskeleton.

(Lucas et al., 2013)

One copy of ena²¹⁰ partially suppresses the neuromuscular junction phenotypes seen in mir-8^Δ2 homozygous mutants.

(Loya et al., 2009)

Khc¹⁶/ena²¹⁰ ; Abl¹/+ triple heterozygous larvae do not show a tail-flipping phenotype and there is a marked reduction in axonal swellings compared to Khc¹⁶/+ ; Abl¹/+ double heterozygous larvae.

(Martin et al., 2005)

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)

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)

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)

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)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

ena^C14-06

(Sano et al., 2012)

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

Images (0)

Mutant

Wild-type

Stocks (2)

Bloomington

8568

wg^Sp-1 Bl¹ ena²¹⁰/CyO

25404

w^*; P{FRT(w^hs)}G13 ena²¹⁰/CyO

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

ena 210

(Stürner et al., 2022)

ena²¹⁰

(Stürner et al., 2022, Feuillette et al., 2020, López-Gay et al., 2020, Wolterhoff et al., 2020, Yaniv et al., 2020, Pinheiro et al., 2017, Lu et al., 2014, Rudrapatna et al., 2014, Lucas et al., 2013, Sano et al., 2012, Gates et al., 2009, Loya et al., 2009, Lyulcheva et al., 2008, Gates et al., 2007, Martin et al., 2005)

enb^2.10

(Bennett and Hoffmann, 1992)

enb²¹⁰

Name Synonyms

Secondary FlyBase IDs

References (32)

Report Sections

Open Close