FB2024_02 , released April 23, 2024
Allele: Dmel\CaMKIIT287D.UAS
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General Information
Symbol
Dmel\CaMKIIT287D.UAS
Species
D. melanogaster
Name
FlyBase ID
FBal0094050
Feature type
allele
Associated gene
Dmel\CaMKII
Associated Insertion(s)
Carried in Construct
P{UAS-CaMKII.T287D}
Also Known As
UAS-CaMKIIT287D, UAS-CaMKII-T287D, UAS-T287D, UASCaMKIIT287D
Key Links
Transgenic product class
missense_variant
(Jin et al., 1998)
Mutagen
Nature of the Allele
Transgenic product class
missense_variant
(Jin et al., 1998)
Mutagen
in vitro construct - regulatory fusion
(Jin et al., 1998)
in vitro construct - coding region fusion
(Jin et al., 1998)
Progenitor genotype
Carried in construct
P{UAS-CaMKII.T287D}
Cytology
Description

UASt regulatory sequences drive expression of CaMKII with the amino acid replacement T287D (this mutation makes the kinase calcium-independent).

(Jin et al., 1998)
Allele components
Component
Use(s)
Regulatory region(s)
UASt
Encoded product / tool
CaMKII
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
      Phenotype Manifest In
      Detailed Description
      Statement
      Reference

      Individuals expressing CaMKIIT287D.UAS under the control of Scer\GAL4CCAP.PU fail to expand their wings after eclosion.

      (Woolums et al., 2020)

      The expression of CaMKIIT287D.Scer\UAS under the control of Scer\GAL4Toll-6-D42 leads to significant increases in the number of type Ib boutons, in the axonal length and in the number of active zones at the larval neuromuscular junction, as compared to controls.

      (Ulian-Benitez et al., 2017)

      Expression of CaMKIIT287D.Scer\UAS under the control of Scer\GAL4VGlut-OK371 results in an increase in bouton number/area for type Ib boutons at the larval neuromuscular junction.

      (Gillespie and Hodge, 2013)

      Flies expressing CaMKIIT287D.Scer\UAS under the control of either Scer\GAL4ey-OK107, Scer\GAL4c305a, Scer\GAL4Mef2.247 or Scer\GAL4CaMKII.7 show normal learning (measured as 2 minute memory) in an olfactory aversive conditioning assay.

      Flies expressing CaMKIIT287D.Scer\UAS under the control of either Scer\GAL4ey-OK107 or Scer\GAL4c305a show severely reduced middle-term memory (measured 3 hours after one cycle of training) in an olfactory aversive conditioning assay. This defect is still seen if expressed is limited to the adult stage using the temperature-sensitive Scer\GAL80ts.αTub84B allele.

      Flies expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4Mef2.247 show normal middle-term memory (measured 3 hours after one cycle of training) in an olfactory aversive conditioning assay.

      Flies expressing CaMKIIT287D.Scer\UAS under the control of either Scer\GAL4ey-OK107 or Scer\GAL4c305a have no long-term memory (measured 24 hours after 5 cycles of spaced training) in an olfactory aversive conditioning assay.

      Flies expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4Mef2.247 show normal long-term memory (measured 24 hours after 5 cycles of spaced training) in an olfactory aversive conditioning assay.

      Flies expressing CaMKIIT287D.Scer\UAS under the control of either Scer\GAL4ey-OK107 or Scer\GAL4c305a have significantly reduced anesthesia-resistant memory (measured 24 hours after 5 cycles of massed training) in an olfactory aversive conditioning assay.

      Flies expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4Mef2.247 show normal anesthesia-resistant memory (measured 24 hours after 5 cycles of massed training) in an olfactory aversive conditioning assay.

      (Malik et al., 2013)

      Expression of CaMKIIT287D.Scer\UAS in the RP2 motor neurons (using the Scer\GAL4eve.RRK driver to drive expression of Scer\FLP1Scer\UAS.cUa which then induces clones of cells expressing Scer\GAL4Act.PU) results in an increase in total dendrite length compared to controls, while dendrite number if not significantly affected. The overall pattern of branching is changed such that there are a greater number of branches closer to the neuronal soma.

      (Timmerman et al., 2013)

      Expression of CaMKIIT287D.Scer\UAS in the motor neurons under the control of Scer\GAL4D42 increases bouton number by approximately 30% and significantly increases motor axon diameter (by approximately 40%).

      CaMKIIT287D.Scer\UAS expression decreases EJP amplitude while having no effect on mEJP amplitude.

      (Chun-Jen Lin et al., 2011)

      Expression of CaMKIIT287D.Scer\UAS under the control of Scer\GAL4how-24B has no effect on the area of the presynaptic terminal at the larval neuromuscular junction.

      The mean amplitude of the excitatory junctional potential (EJP) at the neuromuscular junction is unchanged compared to controls in larvae expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4how-24B. The mean amplitude of spontaneous miniature EJPs at the mutant neuromuscular junction is reduced compared to controls. The quantal content is significantly elevated in the mutant larvae at both 0.4 and 1.5mM extracellular Ca[2+].

      (Morimoto et al., 2010)

      CaMKIIT287D.Scer\UAS expression, under the regulation of Scer\GAL4109(2)80 results in significant increases in dendritic filopodia density in class III neurons. This phenotype is confined to the dendritic compartment of class III neurons, as no filopodia are formed on the axon shafts, and becomes more severe with increasing transgene number. Increasing the transgene number increases the number of filopodia formed without substantially changing the length/number distribution. The CaMKIIT287D.Scer\UAS phenotype does not become apparent until the second instar stage, becoming more prominent later in development. CaMKIIT287D.Scer\UAS expression, under the regulation of Scer\GAL4109(2)80 dramatically increases the numbers of newly formed and disappearing filopodia during development. Larvae expressing CaMKIIT287D.Scer\UAS, under the regulation of Scer\GAL4109(2)80, show a dramatic increase in the post-diffusion turnover of Act5CScer\UAS.T:Avic\GFP with a clear statistically significant shift relative to wild-type.

      (Andersen et al., 2005)

      In neuromuscular junctions of CaMKIIT287D.Scer\UAS; Scer\GAL4Mef2.PR larvae the size of amplitude excitatory postsynaptic potentials (EPSPs) and the amplitude and frequency and kinetics of mini-EPSPs are not significantly different from wild-type. Membrane potential and input resistance of the muscles is also indistinguishable from wild-type. (Data from electrophysiological recordings made from muscle 6 in segment A3 of wandering 3rd instar larvae). The overall numbers of boutons and the numbers of boutons per muscle surface area in CaMKIIT287D.Scer\UAS larvae carrying Scer\GAL4Mhc.PW or Scer\GAL4elav.PLu are not significantly different from wild-type. (Data from neuromuscular junctions of muscles 6 and 7 in segment A3 of wandering 3rd instar larvae). The overall structure of these bouton, the subsynaptic reticulum structure and the number of clear synaptic vesicles appear to be qualitatively wild-type.

      (Haghighi et al., 2003)

      Third instar larvae expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4elav-C155 take significantly longer to roll over after being turned onto their dorsal surface than wild-type larvae. Third instar larvae expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4Appl.G1a do not have a significantly different roll over time than wild-type larvae. A proportion of larvae expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4elav-C155 or CaMKIIT287D.Scer\UAS under the control of Scer\GAL4Appl.G1a are able to locomote while still on their backs (38% and 21% respectively, compared to 2% in controls).

      Evoked excitatory junctional potential amplitudes at the larval neuromuscular junction are unaffected by expression of CaMKIIT287D.Scer\UAS under the control of Scer\GAL4elav-C155. Amplitude and kinetics of spontaneous mEJPs at the larval neuromuscular junction are unaffected by expression of CaMKIIT287D.Scer\UAS under the control of Scer\GAL4Appl.G1a. The frequency of mEJPs is increased in larvae expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4elav-C155 or Scer\GAL4Appl.G1a.

      The total number of boutons at the neuromuscular junction (abdominal segment 2 on muscles 6 and 7) is significantly increased in animals expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4elav-C155 compared to wild type.

      In a subset of larvae expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4elav-C155, evoked excitatory junctional potentials at the neuromuscular junction show a variable delay between the stimulus and initial rise with occasional failures. These delays and failure are not seen in control animals. The delay/failure phenotype is also seen in focal patch recordings made from individual boutons on the muscles of larvae expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4elav-C155.

      (Park et al., 2002)

      Synaptic structure at the larval neuromuscular junction is dramatically altered in flies expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4unspecified at both pre- and postsynaptic sites. The neuromuscular junctions have enlarged synaptic boutons and the distribution pattern of these boutons over the muscle cells is abnormal; the boutons are conglomerated in a smaller area than in wild type and the beaded appearance of the junction which is seen in wild-type larvae is less evident. There is a reduction in the subsynaptic reticulum and an increase in the number of active zones.

      (Koh et al., 1999)

      Flies expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4c362 have an increased reflex response compared to wild-type flies in an assay in which the resistance response from the tibial extensor motor neurons in response to flexing the femorotibial joint is measured. Habituation of this reflex response is blocked in flies expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4c362. The axon projections of the femoral chordotonal organ sensory neurons are normal in flies expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4c362.

      (Jin et al., 1998)
      External Data
      Interactions
      Show genetic interaction network for Enhancers & Suppressors
      Phenotypic Class
      Suppressed by
      Enhancer of
      Statement
      Reference

      Scer\GAL4elav-C155/CaMKIIT287D.UAS is an enhancer of lethal phenotype of paralk5

      (Park et al., 2002)
      Suppressor of
      Statement
      Reference

      CaMKIIT287D.UAS/Scer\GAL4Toll-6-D42 is a suppressor of abnormal neuroanatomy | larval stage phenotype of Df(3L)Exel6092/spz537

      (Ulian-Benitez et al., 2017)

      CaMKIIT287D.UAS/Scer\GAL4Toll-6-D42 is a suppressor of abnormal size | larval stage phenotype of Df(3L)Exel6092/spz537

      (Ulian-Benitez et al., 2017)

      CaMKIIT287D.UAS/Scer\GAL4Toll-6-D42 is a suppressor of abnormal neuroanatomy | larval stage phenotype of Df(3L)Exel6092/spz537, kek634/Df(3R)ED6361

      (Ulian-Benitez et al., 2017)

      CaMKIIT287D.UAS/Scer\GAL4Toll-6-D42 is a suppressor of abnormal size | larval stage phenotype of Df(3L)Exel6092/spz537, kek634/Df(3R)ED6361

      (Ulian-Benitez et al., 2017)

      CaMKIIT287D.UAS/Scer\GAL4Toll-6-D42 is a suppressor of abnormal neuroanatomy | larval stage phenotype of kek634/Df(3R)ED6361

      (Ulian-Benitez et al., 2017)

      CaMKIIT287D.UAS/Scer\GAL4Toll-6-D42 is a suppressor of abnormal neurophysiology phenotype of mGluR112b

      (Chun-Jen Lin et al., 2011)

      CaMKIIT287D.UAS, Scer\GAL80ts.αTub84B, Scer\GAL4Oamb.4.4 is a suppressor of female semi-sterile | recessive phenotype of Oambunspecified

      (Lee et al., 2009)

      CaMKIIT287D.UAS/Scer\GAL4Mhc.PW is a suppressor | partially of abnormal neurophysiology phenotype of GluRIIASP16/Df(2L)cl-h4

      (Haghighi et al., 2003)

      CaMKIIT287D.UAS/Scer\GAL4Mef2.PR is a suppressor | partially of abnormal neurophysiology phenotype of GluRIIASP16/Df(2L)cl-h4

      (Haghighi et al., 2003)

      CaMKIIT287D.UAS is a suppressor | partially of abnormal neurophysiology phenotype of GluRIIAM614R.UAS.Tag:MYC, Scer\GAL4C142

      (Haghighi et al., 2003)

      CaMKIIT287D.UAS, Scer\GAL4Mhc.PW is a suppressor of abnormal neurophysiology phenotype of Rat\CamKII-IAla.UAS, Scer\GAL4Mhc.PW

      (Haghighi et al., 2003)
      NOT Suppressor of
      Phenotype Manifest In
      Suppressed by
      Suppressor of
      NOT Suppressor of
      Additional Comments
      Genetic Interactions
      Statement
      Reference

      The expression of CaMKIIT287D.Scer\UAS under the control of Scer\GAL4Toll-6-D42 suppresses the decreased type I bouton number observed at the larval neuromuscular junction of kek634/Df(3R)ED6361 transheterozygotes; this expression also suppresses the decreased axonal length observed at the larval neuromuscular junction of either spz537/Df(3L)Exel6092 single transheterozygotes or spz537/Df(3L)Exel6092, kek634/Df(3R)ED6361 double transheterozygotes.

      (Ulian-Benitez et al., 2017)

      Co-expression of CASKScer\UAS.cBa suppresses the increase in bouton number/area seen for type Ib boutons at the neuromuscular junction in larvae expressing CaMKIIT287D.Scer\UAS under the control of Scer\GAL4VGlut-OK371.

      (Gillespie and Hodge, 2013)

      In larvae co-expressing CaMKIIT287D.Scer\UAS and Pi3K92ED954A.Scer\UAS.T:Hsap\MYC under the control of Scer\GAL4D42, the CaMKIIT287D.Scer\UAS-dependent increase in bouton number is completely suppressed and is decreased to a value indistinguishable from that conferred by expression of Pi3K92ED954A.Scer\UAS.T:Hsap\MYC alone.

      The axon diameter increase seen upon expression of CaMKIIT287D.Scer\UAS under the control of Scer\GAL4D42 is suppressed by a Fak56DCG1 mutant background.

      CaMKIIT287D.Scer\UAS expression completely suppresses the hyper-excitability found in mGluRA112b mutants to the level found upon expression of CaMKIIT287D.Scer\UAS in a wild-type background.

      A Fak56DCG1 background completely suppresses the increased synapse number conferred by CaMKIIT287D.Scer\UAS expression. Synapse number in these double mutants is indistinguishable from that in Fak56DCG1 single mutants.

      (Chun-Jen Lin et al., 2011)

      Expression of CaMKIIT287D.Scer\UAS under the control of Scer\GAL4Oamb.4.4, using Scer\GAL80ts.αTub84B to limit expression to 3 days prior to mating, suppresses the ovulation phenotype seen in Oambunspecified homozygotes.

      Expression of CaMKIIT287D.Scer\UAS under the control of Scer\GAL4elav.PU, using Scer\GAL80ts.αTub84B to limit expression to 3 days prior to mating, fails to suppress the ovulation phenotype seen in Oambunspecified homozygotes.

      (Lee et al., 2009)

      Excitatory postsynaptic potential (EPSP) amplitudes in the neuromuscular junctions of GluRIIASP16/Df(2L)cl-h4 larvae are decreased by a third by CaMKIIT287D.Scer\UAS; Scer\GAL4Mef2.PR, but quantal size is unaffected, resulting in a significant decrease (p < 0.001) in quantal content (a 57% decrease (corrected for nonlinear summation)). Similar results are seen when Scer\GAL4Mhc.PW is used in place of Scer\GAL4Mef2.PR. (Data from electrophysiological recordings made from muscle 6 in segment A3 of wandering 3rd instar larvae).

      (Haghighi et al., 2003)

      Expression of CaMKIIT287D.Scer\UAS under the control of Scer\GAL4elav-C155 enhances the lethality of paralk5.

      (Park et al., 2002)

      The rescue of the dlg17 neuromuscular junction defects by dlg1S48A.Scer\UAS.T:Avic\GFP expressed under the control of Scer\GAL4unspecified is unaltered by expression of CaMKIIT287D.Scer\UAS in the postsynaptic muscles.

      (Koh et al., 1999)
      Xenogenetic Interactions
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      Mutant
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      Stocks (2)
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      External Crossreferences and Linkouts ( 0 )
      Synonyms and Secondary IDs (2)
      Reported As
      Symbol Synonym
      CaMKIIT287D.Scer\UAS
      CaMKIIT287D.UAS
      Name Synonyms
      Secondary FlyBase IDs
        References (25)