FlyBase Allele Report: Dmel\Tak1[2]

General Information

Symbol

Dmel\Tak1²

Species

D. melanogaster

Name

FlyBase ID

FBal0126474

Feature type

allele

Associated gene

Dmel\Tak1

Associated Insertion(s)

Carried in Construct

Also Known As

dTak1²

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

Mutagen

ethyl methanesulfonate

(Vidal et al., 2001)

Progenitor genotype

Cytology

Description

The Tak1² mutation is within the kinase domain of the expressed product.

(Delaney et al., 2006)

Amino acid replacement: E53term.

(Vidal et al., 2001)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

X:20,523,271..20,523,271 [-]

Nucleotide change:

G20523271T

Amino acid change:

E53term | Tak1-PA

Reported amino acid change:

E53term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

(Vidal et al., 2001)

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

abdominal segment motor neuron | third instar larval stage

(Harris et al., 2018)

abdominal segment motor neuron | third instar larval stage (with Df(1)BSC645)

(Harris et al., 2018)

abdominal segment motor neuron | third instar larval stage (with Tak1¹⁷⁹)

(Harris et al., 2018)

embryonic/larval neuromuscular junction | third instar larval stage

(Harris et al., 2018)

embryonic/larval neuromuscular junction | third instar larval stage (with Df(1)BSC645)

(Harris et al., 2018)

embryonic/larval neuromuscular junction | third instar larval stage (with Tak1¹⁷⁹)

(Harris et al., 2018)

presynaptic active zone

(Harris et al., 2018)

synaptic vesicle

(Harris et al., 2018)

synaptic vesicle, readily releasable pool

(Harris et al., 2018)

type I bouton | third instar larval stage

(Harris et al., 2018)

ventral midline of embryo | embryonic stage 13 | conditional

(Barros and Bossing, 2021)

Detailed Description

Statement

Reference

Tak1²/Tak1² prevents the regenerative mitosis induced by physical ablation of a section of the embryonic ventral midline.

(Barros and Bossing, 2021)

Motor neurons in either Tak1²/Tak1² or Tak1²/Df(1)BSC645 third instar larvae show a decrease in baseline neurotransmission, with significantly reduced mEPSP (mini excitatory postsynaptic potential) and EPSP (excitatory postsynaptic potential) amplitudes, but no change in quantal content compared to controls. Tak1²/Tak1² motor neurons display a significantly reduced mEPSP frequency.

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, Tak1²/Tak1² motor neurons show a decrease in the initial EPSC (excitatory postsynaptic current) amplitude of a stimulus train, followed by facilitation, with significant increases in the cumulative EPSC amplitude and size of the readily releasable synaptic vesicle pool, accompanied by a dramatic and consistent decrease in presynaptic release probability compared to controls. Facilitation is blunted in response to a stimulus train in the presence of a calcium chelator (EGTA-AM). Recovery from strong synaptic depression at elevated extracellular calcium is also impaired. There is no change in EPSC amplitude when a single-stimulus protocol is applied in the presence of EGTA-AM.

Motor neurons in Tak1²/Tak1² third instar larvae display a moderate reduction in type I bouton number and a corresponding increase in active zone density (but a similar number of active zones) compared to controls. There is a significant decrease in the overall number of synaptic vesicles at release sites and the number of docked vesicles, accompanied by an increased inter-vesicle distance. Following high-frequency stimulation, the total numbers of synaptic vesicles and docked vesicles are restored and resemble control levels.

(Harris et al., 2018)

Tak1²/Tak1² adult flies have significantly reduced survival in response to Gram-negative bacteria (Erwinia carotovora carotovora 15), compared to controls.

(Liu et al., 2016)

Tak1² mutant exhibit defects in immune response. More than half of males die over the course of a week after E.coli infection. Tak1² heterozygotes appear normal, but homozygotes show increased susceptibility to E.coli.

Expression of Tak1^{K46R.M.Scer\UAS} under the control of Scer\GAL4^da.G32 modestly increases susceptibility of Tak1²/+ females to E.coli.

(Stronach et al., 2014)

Tak1² mutant larvae do not exhibit a melanotic phenotype in the posterior hindgut either under normal food conditions or when raised on food containing 0.1M or 0.2M NaCl.

(Seisenbacher et al., 2011)

Mutants show reduced survival compared to control flies after infection with one of K.pneumoniae or E.cloacae by septic injury.

Mutants show reduced survival compared to control flies after oral infection with P.aeruginosa.

Mutants show normal sensitivity to infection with E.faecalis or S.aureus.

(Bergeret et al., 2008)

Mutant flies show strong sensitivity to infection with P.aeruginosa or E.coli by septic injury.

(Avet-Rochex et al., 2007)

Flies are susceptible to Gram-negative bacterial infection.

(Vidal et al., 2001)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Tak1² has abnormal neurophysiology | third instar larval stage phenotype, enhanceable by GluRIIA^SP16/GluRIIA^SP16

(Harris et al., 2018)

NOT suppressed by

Statement

Reference

Tak1² has abnormal immune response phenotype, non-suppressible by slpr::Tak1^{SAAATCt.UASp.Tag:HA}/Scer\GAL4^da.G32

(Stronach et al., 2014)

Tak1² has abnormal immune response phenotype, non-suppressible by Scer\GAL4^da.G32/slpr::Tak1^{STCt.UASp.Tag:HA}

(Stronach et al., 2014)

Tak1² has abnormal immune response phenotype, non-suppressible by Scer\GAL4^da.G32/slpr::Tak1^{STK.UASp.Tag:HA}

(Stronach et al., 2014)

Tak1² has abnormal immune response phenotype, non-suppressible by slpr::Tak1^{TSK.UASp.Tag:HA}/Scer\GAL4^da.G32

(Stronach et al., 2014)

Tak1² has abnormal immune response phenotype, non-suppressible by Scer\GAL4^da.G32/slpr::Tak1^{TSAAA.UASp.Tag:HA}

(Stronach et al., 2014)

Suppressor of

Statement

Reference

Tak1² is a suppressor | partially of melanotic mass phenotype | larval stage | nutrition conditional phenotype of MAPk-Ak2^Δ43

(Seisenbacher et al., 2011)

NOT Suppressor of

Statement

Reference

Tak1²/Tak1² is a non-suppressor of abnormal neurophysiology | third instar larval stage phenotype of GluRIIA^SP16

(Harris et al., 2018)

Other

Statement

Reference

Scer\GAL4^da.G32, Tak1², slpr::Tak1^{STCt.UASp.Tag:HA} has abnormal immune response phenotype

(Stronach et al., 2014)

Phenotype Manifest In

Enhanced by

Statement

Reference

Tak1² has abdominal segment motor neuron | third instar larval stage phenotype, enhanceable by GluRIIA^SP16/GluRIIA^SP16

(Harris et al., 2018)

Tak1² has embryonic/larval neuromuscular junction | third instar larval stage phenotype, enhanceable by GluRIIA^SP16/GluRIIA^SP16

(Harris et al., 2018)

Suppressor of

Statement

Reference

Tak1² is a suppressor | partially of embryonic/larval hindgut | posterior | larval stage | nutrition conditional phenotype of MAPk-Ak2^Δ43

(Seisenbacher et al., 2011)

Tak1² is a suppressor of eye phenotype of Scer\GAL4^GMR.PU, egr^{ecto-60.UAS.Tag:HA,Tag:FLAG}

(Narasimamurthy et al., 2009)

Tak1² is a suppressor of eye phenotype of Scer\GAL4^GMR.PU, egr^UAS.cMa

(Narasimamurthy et al., 2009)

NOT Suppressor of

Statement

Reference

Tak1²/Tak1² is a non-suppressor of abdominal segment motor neuron | third instar larval stage phenotype of GluRIIA^SP16

(Harris et al., 2018)

Tak1²/Tak1² is a non-suppressor of embryonic/larval neuromuscular junction | third instar larval stage phenotype of GluRIIA^SP16

(Harris et al., 2018)

Additional Comments

Genetic Interactions

Statement

Reference

Motor neurons in Tak1², GluRIIA^SP16 double mutant third instar larvae display characteristics of long-term presynaptic homeostatic plasticity: reduced mEPSP (mini excitatory postsynaptic potential) amplitudes (but not EPSP; excitatory postsynaptic potential) accompanied by increased quantal content as compared to single Tak1² controls, but similar to GluRIIA^SP16 single mutants.

(Harris et al., 2018)

Expression of slpr::Tak1^{SAAATCt.Scer\UAS.P\T.T:Ivir\HA1} under the control of Scer\GAL4^da.G32 does not suppress the increased susceptibility to E.coli challenge seen in Tak1²/Y males. Expression of slpr::Tak1^{SAAATCt.Scer\UAS.P\T.T:Ivir\HA1} modestly increases susceptibility of Tak1²/+ females to E.coli.

Expression of slpr::Tak1^{STCt.Scer\UAS.P\T.T:Ivir\HA1} under the control of Scer\GAL4^da.G32 does not suppress the increased susceptibility to E.coli challenge seen in Tak1²/Y males. Expression of slpr::Tak1^{STCt.Scer\UAS.P\T.T:Ivir\HA1} does not increase susceptibility of Tak1²/+ females to E.coli.

Expression of slpr::Tak1^{STK.Scer\UAS.P\T.T:Ivir\HA1} under the control of Scer\GAL4^da.G32 does not suppress the increased susceptibility to E.coli challenge seen in Tak1²/Y males. Expression of slpr::Tak1^{STK.Scer\UAS.P\T.T:Ivir\HA1} does not increase susceptibility of Tak1²/+ females to E.coli.

Expression of slpr::Tak1^{TSK.Scer\UAS.P\T.T:Ivir\HA1} under the control of Scer\GAL4^da.G32 does not suppress the increased susceptibility to E.coli challenge seen in Tak1²/Y males. Expression of slpr::Tak1^{TSK.Scer\UAS.P\T.T:Ivir\HA1} does not increase susceptibility of Tak1²/+ females to E.coli.

Expression of slpr::Tak1^{TSAAA.Scer\UAS.P\T.T:Ivir\HA1} under the control of Scer\GAL4^da.G32 does not suppress the increased susceptibility to E.coli challenge seen in Tak1²/Y males. Expression of slpr::Tak1^{TSAAA.Scer\UAS.P\T.T:Ivir\HA1} does not increase susceptibility of Tak1²/+ females to E.coli.

Expression of slpr^{AAA.Scer\UAS.P\T.T:Ivir\HA1} under the control of Scer\GAL4^da.G32 does not increase susceptibility of Tak1²/+ females to E.coli challenge.

(Stronach et al., 2014)

Tak1² partially suppresses the "black dot" phenotype seen in the hindgut of MAPk-Ak2^Δ43 larvae raised on either 0.1M or 0.2M NaCl.

(Seisenbacher et al., 2011)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Tak1¹⁷⁹

(Delaney et al., 2006)

Not rescued by

Tak1[+]/Tak1² is not rescued by Scer\GAL4^da.G32/Tak1^{Ct.UASp.Tag:HA}

(Stronach et al., 2014)

Comments

Expression of Tak1^{Ct.Scer\UAS.P\T.T:Ivir\HA1} under the control of Scer\GAL4^da.G32 does not rescue the increased susceptibility to E.coli challenge seen in Tak1²/Y males. Expression of Tak1^{Ct.Scer\UAS.P\T.T:Ivir\HA1} under the control of either Scer\GAL4^da.G32 or Scer\GAL4^r4 does not increase susceptibility of Tak1²/+ females to E.coli.

(Stronach et al., 2014)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

26272

y¹ w^* Tak1²

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

TAK1²

(Seisenbacher et al., 2011, Avet-Rochex et al., 2007)

Tak1²

(Shen et al., 2022, Liaw and Chiang, 2019, Harris et al., 2018, Nandy et al., 2018, Chen et al., 2017, Liu et al., 2016, Stronach et al., 2014)

dTAK1²

(Narasimamurthy et al., 2009, Bergeret et al., 2008, Delaney et al., 2006)

dTak1²

(Bangi et al., 2012)

Name Synonyms

Secondary FlyBase IDs

References (15)

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