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General Information
Symbol
Rat\CamKII-IAla.UAS
Species
R. unknown
Name
FlyBase ID
FBal0086889
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
UAS-Ala, UASAla
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Carried in construct
Cytology
Nature of the lesion
Statement
Reference

UAS regulatory sequences drive expression of the 'ala' inhibitor peptide that is specific for CaM kinase (this inhibitor is a synthetic peptide based on the Rat\CamKII-I autoregulatory domain, carrying an Ala in place of the Thr that is normally autophosphorylated).

Allele components
Product class / Tool use(s)
Encoded product / tool
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
Comments on Models/Modifiers Based on Experimental Evidence ( 0 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Expression of Rat\CamKII-IAla.Scer\UAS under the control of Scer\GAL4how-24B has no effect on the amplitude of evoked activity events visualized by the Avic\GFPSynapGCaMP6f.Mhc sensor neither does it affect density of active synapses or variability in the release probability at either motor neuron Is or Ib input but it increases both the single-synapse release probability and quantal density per stimulus at Ib synapses while neither of these parameters is affected at Is synapses.

The expression of Rat\CamKII-IAla.Scer\UAS under the control of Scer\GAL4Toll-6-D42 leads to significant decreases in both the axonal length and the number of active zones at the larval neuromuscular junction, as compared to controls.

Expression of Rat\CamKII-IAla.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 a significant decrease in the number of dendritic branches and total dendrite length compared to controls. The overall pattern of branching is changed such that there are a greater number of branches closer to the neuronal soma.

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

At 1.5mM extracellular Ca[2+], the mean amplitude of the excitatory junctional potential (EJP) at the neuromuscular junction is increased compared to control larvae in larvae expressing Rat\CamKII-IAla.Scer\UAS under the control of Scer\GAL4how-24B. However, at 0.75mM extracellular Ca[2+], the mean EJP at the mutant neuromuscular junction is not significantly different from that of controls. The mean amplitude of spontaneous miniature EJPs at the mutant neuromuscular junction is unchanged compared to controls. The quantal content is significantly elevated in the mutant larvae at 1.5mM extracellular Ca[2+].

Expression of Rat\CamKII-IAla.Scer\UAS (either alone or under the control of Scer\GAL4hs.2sev) has little or no effect on free-running circadian period.

In neuromuscular junctions of Rat\CamKII-IAla.Scer\UAS larvae carrying Scer\GAL4Mef2.PR or Scer\GAL4Mhc.PW, but not Scer\GAL4elav.PLu, excitatory postsynaptic potential (EPSP) amplitude is increased by 20% compared to wild-type (p < 0.001) resulting in a 20% increase (p < 0.005) in quantal content. However, the amplitude and frequency and kinetics of mini-EPSPs are not significantly different from wild-type and neither are membrane potential and input resistance of the muscles. (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 Rat\CamKII-IAla.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. However, boutons in Rat\CamKII-IAla.Scer\UAS; Scer\GAL4Mhc.PW but not Rat\CamKII-IAla.Scer\UAS; Scer\GAL4elav.PLu larvae, display an unusual invagination of the presynaptic membrane at active zones and have a 60% increase in the number of t-bars per active zone (p < 0.001).

Flies expressing Rat\CamKII-IAla.Scer\UAS under the control of one of Scer\GAL429BD, Scer\GAL430Y, Scer\GAL4Tab2-201Y, Scer\GAL4OK348, Scer\GAL440B, Scer\GAL4MJ162A, Scer\GAL4MJ146, Scer\GAL4MJ63 or Scer\GAL4MJ94 show normal locomotor activity. Expression of Rat\CamKII-IAla.Scer\UAS under the control of Scer\GAL4Tab2-201Y or Scer\GAL4MJ94 results in males with an abnormal courtship response during training with a mated female (wild-type males show a decrement in courtship during training, with the ratio of the final courtship index/initial courtship index being approximately 0.5. This ratio is significantly increased in the mutant flies). This phenotype is seen both in the presence and absence of visual input. Expression of Rat\CamKII-IAla.Scer\UAS under the control of Scer\GAL4OK348, Scer\GAL4MJ63 or Scer\GAL440B results in males with an abnormal courtship response during training with a mated female (wild-type males show a decrement in courtship during training, with the ratio of the final courtship index/initial courtship index being approximately 0.5. This ratio is significantly increased in the mutant flies). This phenotype is only seen in the presence of visual input. Expression of Rat\CamKII-IAla.Scer\UAS under the control of Scer\GAL4MJ162A or Scer\GAL4MJ146 results in males with an abnormal courtship response during training with a mated female (wild-type males show a decrement in courtship during training, with the ratio of the final courtship index/initial courtship index being approximately 0.5. This ratio is significantly increased in the mutant flies). This phenotype is only seen in the absence of visual input. Expression of Rat\CamKII-IAla.Scer\UAS under the control of one of Scer\GAL429BD, Scer\GAL430Y, Scer\GAL4Tab2-201Y, Scer\GAL4OK348, Scer\GAL440B, Scer\GAL4MJ162A, Scer\GAL4MJ146, Scer\GAL4MJ63 or Scer\GAL4MJ94 does not disrupt memory formation in males trained in a courtship conditioning assay under white light. However, in the absence of visual input (red light), expression of Rat\CamKII-IAla.Scer\UAS under the control of one of Scer\GAL429BD, Scer\GAL430Y, Scer\GAL4Tab2-201Y, Scer\GAL4OK348 or Scer\GAL4MJ63 blocks formation of memory in this assay.

Expression of Rat\CamKII-IAla.Scer\UAS under the control of Scer\GAL4unspecified at both pre- and postsynaptic sites at the larval neuromuscular junction does not result in gross morphological changes. However, there is a significant alteration in bouton ultrastructure; the SSR appears more extensive than wild type. The number of active zones in type I boutons is similar to wild type.

Flies expressing Rat\CamKII-IAla.Scer\UAS under the control of Scer\GAL4c362 have a decreased 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. The initial reflex response is only 33% of the response in control flies. Habituation of this reflex response is blocked. The axon projections of the femoral chordotonal organ sensory neurons are normal in flies expressing Rat\CamKII-IAla.Scer\UAS under the control of Scer\GAL4c362.

Scer\GAL4MJ85b-mediated expression in males does not cause a block in memory, even in the apparent absence of learning, in courtship behaviour assays.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference

The co-expression of Rat\CamKII-IAla.Scer\UAS partially suppresses the lamina vacuolization induced by the expression of Hsap\MAPTScer\UAS.cWa under the control of Scer\GAL4GMR.PU.

Co-expression of Adf1S64D.S184D.Scer\UAS.T:Zzzz\FLAG partially suppresses the reduced number of dendritic branches seen in RP2 motor neurons expressing Rat\CamKII-IAla.Scer\UAS (the Scer\GAL4eve.RRK driver is used to drive expression of Scer\FLP1Scer\UAS.cUa which then induces clones of cells expressing Scer\GAL4Act.PU).

The increase in quantal content and excitatory postsynaptic potential (EPSP) amplitude at neuromuscular junctions seen in Rat\CamKII-IAla.Scer\UAS; Scer\GAL4Mhc.PW larvae is suppressed by CaMKIIT287D.Scer\UAS.

Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Symbol Synonym
CamKII-IAla.UAS
Rat\CamKII-IAla.Scer\UAS
Rat\CamKII-IAla.UAS
Name Synonyms
Secondary FlyBase IDs
    References (16)