FlyBase Allele Report: Dmel\tok[E1]

General Information

Symbol

Dmel\tok^E1

Species

D. melanogaster

Name

FlyBase ID

FBal0191955

Feature type

allele

Associated gene

Dmel\tok

Associated Insertion(s)

Carried in Construct

Also Known As

tlr^E1

Key Links

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

Progenitor genotype

Cytology

Description

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

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 ( 0 )

Disease

Interaction

References

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal neuroanatomy | embryonic stage (with Df(3R)tld-γ1)

(Serpe and O'Connor, 2006)

abnormal neuroanatomy | embryonic stage (with tok^Δ2-41)

(Serpe and O'Connor, 2006)

abnormal neuroanatomy | larval stage (with Df(3R)tld-γ1)

(Serpe and O'Connor, 2006)

abnormal neuroanatomy | larval stage (with tok^Δ2-41)

(Serpe and O'Connor, 2006)

lethal | larval stage (with tok^Δ2-41)

(Serpe et al., 2005)

lethal | pupal stage (with tok^Δ2-41)

(Serpe et al., 2005)

lethal - all die before end of larval stage (with Df(3R)tld-γ1)

(Serpe and O'Connor, 2006)

lethal - all die before end of larval stage (with tok^Δ2-41)

(Serpe and O'Connor, 2006)

some die during larval stage (with Df(3R)tld-γ1)

(Serpe and O'Connor, 2006)

some die during larval stage (with tok^Δ2-41)

(Serpe and O'Connor, 2006)

Phenotype Manifest In

Detailed Description

Statement

Reference

tok^Δ2-41/tok^E1 embryos have a normal CNS appearance overall. However, the embryos show a phenotype of variable penetrance in which the Fas2-positive longitudinal bundles are wavy and irregular and the outer bundle is discontinuous or missing. These embryos also show a variety of guidance defects, including delay in intersegmental nerve growth and defective terminal arbor morphology, SNa stalling and additional branching and the failure of SNb to reach ventral muscle targets. tok^E1/Df(3R)tld-γ1 embryos also show these axon guidance defects.

The axon guidance defects of tok^Δ2-41/tok^E1 and tok^E1/Df(3R)tld-γ1 mutants persist until larval stages when the animals begin to die. Although muscles 6 and 7 of these mutants show relatively normal NMJs, there is abnormal innervation in the cleft between muscles 12 and 13 and the innervation on muscle 12 is entirely absent, reduced or misrouted.

(Serpe and O'Connor, 2006)

Rare tok^Δ2-41/tok^E1 escapers exhibit loss of the crossveins in the wing.

(Serpe et al., 2005)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Phenotype Manifest In

Suppressed by

Statement

Reference

tok^Δ2-41/tok^E1 has crossvein phenotype, suppressible by sog^YL26/sog^P129D

(Serpe et al., 2005)

tok^Δ2-41/tok^E1 has crossvein phenotype, suppressible | partially by sog[+]/sog^YL26

(Serpe et al., 2005)

NOT suppressed by

Statement

Reference

tok^Δ2-41/tok^E1 has crossvein phenotype, non-suppressible by Scer\GAL4^A9/tld^UAS.cHa

(Serpe et al., 2005)

tok^Δ2-41/tok^E1 has crossvein phenotype, non-suppressible by tld^UAS.cHa/Scer\GAL4^da.G32

(Serpe et al., 2005)

Additional Comments

Genetic Interactions

Statement

Reference

sog^YL26/+; tok^Δ2-41/tok^E1 escapers exhibit partial posterior crossveins with significantly more crossvein material than tok^Δ2-41/tok^E1 escapers. Further, crossveins are almost completely restored in sog^YL26/sog^P129D; tok^Δ2-41/tok^E1 animals. Expression of tld^Scer\UAS.cHa under the control of Scer\GAL4^da.G32 or Scer\GAL4^A9 fails to rescue the posterior crossvein phenotype of tok^Δ2-41/tok^E1 mutants.