FB2025_01 , released February 20, 2025
Allele: Dmel\Tak1179
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General Information
Symbol
Dmel\Tak1179
Species
D. melanogaster
Name
FlyBase ID
FBal0194041
Feature type
allele
Associated gene
Dmel\Tak1
Associated Insertion(s)
Carried in Construct
Key Links
Genomic Maps

Allele class

loss of function allele

Mutagen
Nature of the Allele
Allele class

loss of function allele

(Delaney et al., 2006)
Mutagen
ethyl methanesulfonate
(Delaney et al., 2006)
Progenitor genotype
Cytology
Description

Amino acid replacement: G31D.

(Delaney et al., 2006)

The G31D mutation is within the ATP binding motif in the kinase subdomain I region and results in a kinase-dead product.

(Delaney et al., 2006)
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
point_mutation
X:20,523,336..20,523,336 [-]
Nucleotide change:

G20523336A

Amino acid change:

G31E | Tak1-PA

Reported amino acid change:

G31D

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change. The lesion is reported as a G to D mutation, however the a single base mutation in the second base of the codon leads to either a Gly to Asp or Gly to Glu mutation, depending on the third base of the codon. Assuming the mutation is a single base change, in the reference genome sequence, the change is Gly to Glu.

(Delaney et al., 2006)
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
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Motor neurons in Tak1179/Tak1179 third instar larvae show a decrease in baseline neurotransmission, with significantly reduced mEPSP (mini excitatory postsynaptic potential) and EPSP (excitatory postsynaptic potential) amplitudes, mEPSP frequency and baseline quantal content compared to controls.

      Following high-frequency stimulation, Tak12/Tak12 and Tak12/Tak1179 larvae display profound short-term facilitation, in contrast to the synaptic depression characteristic of controls. Under this protocol, Tak1179/Tak1179 motor neurons show a decrease in the initial EPSC (excitatory postsynaptic current) amplitude of a stimulus train, followed by facilitation and a dramatic and consistent decrease in presynaptic release probability. Recovery from strong synaptic depression at elevated extracellular calcium is also impaired. There is no effect on cumulative EPSC (excitatory postsynaptic current) amplitude or size of the readily releasable synaptic vesicle pool.

      Motor neurons in Tak1179/Tak1179 third instar larvae display a small but significant increase in type I bouton number and a similar number and density of active zones compared to controls. There is a significant decrease in the overall number of synaptic vesicles at release sites (but not the number of docked vesicles), accompanied by an increased inter-vesicle distance.

      (Harris et al., 2018)

      The number of synaptic boutons at neuromuscular junctions in heterozygous Tak1179 larvae is similar to that of wild-type.

      (West et al., 2015)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Enhanced by
      Suppressor of
      Statement
      Reference

      Tak1[+]/Tak1179 is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Rab81/Rab8B229

      (West et al., 2015)
      NOT Suppressor of
      Statement
      Reference

      Tak1179/Tak1179 is a non-suppressor of abnormal neurophysiology | third instar larval stage phenotype of GluRIIASP16

      (Harris et al., 2018)
      Phenotype Manifest In
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      Motor neurons in Tak1179, GluRIIASP16 double mutant third instar larvae display characteristics of long-term presynaptic homeostatic plasticity: reduced mEPSP (mini excitatory postsynaptic potential) and increased quantal content as compared to single Tak1179 controls, but similar to GluRIIASP16 single mutants. Additionally, motor neurons have reduced EPSP (excitatory postsynaptic potential) amplitudes compared to either single mutant.

      (Harris et al., 2018)
      Xenogenetic Interactions
      Statement
      Reference
      Complementation and Rescue Data
      Images (0)
      Mutant
      Wild-type
      Stocks (1)
      Notes on Origin
      Discoverer

      Selected as: an adult viable mutation on the X chromosome that impairs expression of the Dpt gene in response to bacterial challenge.

      (Delaney et al., 2006)
      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (5)
      Reported As
      Symbol Synonym
      TAK1179
      (West et al., 2015)
      Tak1179
      (Liaw and Chiang, 2019, Yang et al., 2019, Harris et al., 2018)
      dTAK1179
      (Delaney et al., 2006)
      dTAK179
      (Collu et al., 2018)
      fb(x)17
      (Delaney et al., 2006)
      Name Synonyms
      Secondary FlyBase IDs
        References (6)