A Database of Drosophila Genes & Genomes

FB2013_03, released May 7th, 2013
 

Allele Rat\CamKII-IAla.hs

General Information
SymbolRat\CamKII-IAla.hsSpeciesR. unknown
NameFlyBase IDFBal0048075
Feature typealleleAssociated geneRat\CamKII-I
Allele class
Mutagenin vitro construct - regulatory fusion
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Description
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FB2013_03
FB2013_02
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Allele class
Mutagen
Mutations Mapped to the Genome
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Associated Sequence Data
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Construct: Expression of a synthetic peptide, carrying an Ala in place of the Thr that is autophosphorylated, is driven by an Hsp70 promoter.
Carried in construct
Cytology
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Expression of Rat\CamKII-I[Ala.hs] in motor neurons under the control of Scer\GAL4[D42] decreases synapse number about two-fold.
Expression of Rat\CamKII-IAla.hs (either alone or under the control of Scer\GAL4hs.2sev) has little or no effect on free-running circadian period.
Animals carrying Rat\CamKII-IAla.hs show an approximately 40% increase in bouton number at the neuromuscular junction.
Neurons expressing Rat\CamKII-I[Ala.hs] typically display prolonged action potential waveforms and abnormal spontaneous activity. The spike duration (the width of the at the inflection point during an action potential take-off in a spike train) is substantially prolonged in Rat\CamKII-I[Ala.hs] neurons. During sustained step current injection, all-or-none spikes in the tonic and adaptive categories in Rat\CamKII-I[Ala.hs] neurons exhibit a progressive decrease in spike size (along with an increase in spike duration over the period of stimulation), in contrast to the well-maintained spike shape in wild-type cells. A subpopulation of Rat\CamKII-I[Ala.hs] neurons fire highly irregular spike pattern in response to current injection. Long-lasting spontaneous bursting activity with sporadic occurrence and varying frequency is observed in 25-30% of Rat\CamKII-I[Ala.hs] neurons compared with only 5% in wild-type cells, although the resting membrane potentials within spontaneous spike trains are also prolonged. When Rat\CamKII-I[Ala.hs] neurons are simulated by step current injections, the firing pattern, in particular the number of spikes in each spike train, varied to a much greater extent than that in wild-type cells.
Males do not show a block in memory, even in the apparent absence of learning, in courtship behaviour assays.
Homozygotes fail to court females. Physiological studies reveal supernumerary synaptic discharges.
Individuals exhibit clear free-running locomotor activity rhythms.
Expression of P{CamKII-IAla.hs} with or without heat shock causes an impaired associative conditioning behavioural paradigm. Altered short term plasticity in synaptic transmission along with abnormal nerve terminal sprouting and directionality of outgrowth. Excitatory junctional currents (EJCs) are greater than normal.
Transformed flies fail to learn normally in two behavioural plasticity paradigms: acoustic priming (a nonassociative measure of sensitization) and courtship conditioning (a measure of associative learning).
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Co-expression of Pi3K92E[Scer\UAS.T:Hsap\MYC,T:Hsap\CAAX] in motor neurons with Rat\CamKII-I[Ala.hs], both under the control of Scer\GAL4[D42], suppresses the Rat\CamKII-I[Ala.hs]-dependent decrease in synapse number. Synapse number is significantly increased in these double mutants and is indistinguishable from synapse number in larvae expressing Pi3K92E[Scer\UAS.T:Hsap\MYC,T:Hsap\CAAX] alone.
Flies expressing Rat\CamKII-I[Ala.hs] under the control of Scer\GAL4[Oamb.4.4] in a Oamb[unspecified] heterozygous background show significantly reduced ovulation levels compared to controls. Reduced ovulation levels are also seen when Scer\GAL80[ts.αTub84B] is used to limit expression to 3 days prior to mating.
Flies expressing both Mmmm\PVScer\UAS.T:Hsap\MYC and Rat\CamKII-IAla.hs under the control of Scer\GAL4P2.4.Pdf exhibit period lengthening that is significantly different from controls.
Animals carrying Rat\CamKII-IAla.hs which are also mutant for mysb9 show an approximately 20% increase in bouton number at the neuromuscular junction. Animals carrying Rat\CamKII-IAla.hs which are also mutant for mysts1 show an approximately 16% increase in bouton number at the neuromuscular junction.
eag1/Rat\CamKII-IAla.hs individuals also fail to court.
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Can be expressed without heat shock.
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Reported As
Symbol Synonym
CamKII-IAla.hs
 
Rat\CamKII-IAla.hs
 
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Secondary FlyBase IDs
hide References ( 14 )
Research paper
Vonhoff et al., 2013, Development 140(3): 606--616
Temporal coherency between receptor expression, neural activity and AP-1-dependent transcription regulates Drosophila motoneuron dendrite development. [FBrf0220342]
Chun-Jen Lin et al., 2011, Genetics 188(3): 601--613
The Metabotropic Glutamate Receptor Activates the Lipid Kinase PI3K in Drosophila Motor Neurons Through the Calcium/Calmodulin-Dependent Protein Kinase II and the Nonreceptor Tyrosine Protein Kinase DFak. [FBrf0214227]
Lee et al., 2009, PLoS ONE 4(3): e4716
The octopamine receptor OAMB mediates ovulation via Ca2+/calmodulin-dependent protein kinase II in the Drosophila oviduct epithelium. [FBrf0207515]
Harrisingh et al., 2007, J. Neurosci. 27(46): 12489--12499
Intracellular Ca[2+] Regulates Free-Running Circadian Clock Oscillation In Vivo. [FBrf0204998]
Dunn and Mercier, 2005, Peptides 26(2): 269--276
Synaptic modulation by a Drosophila neuropeptide is motor neuron-specific and requires CaMKII activity. [FBrf0184231]
Beumer et al., 2002, Development 129(14): 3381--3391
Integrins regulate DLG/FAS2 via a CaM kinase II-dependent pathway to mediate synapse elaboration and stabilization during postembryonic development. [FBrf0151260]
Yao and Wu, 2001, J. Neurophysiol. 85(4): 1384--1394
Distinct roles of CaMKII and PKA in regulation of firing patterns and k(+) currents in Drosophila neurons. [FBrf0135857]
Zhou et al., 1999, Neuron 22(4): 809--818
A dynamically regulated 14-3-3, Slob, and Slowpoke potassium channel complex in Drosophila presynaptic nerve terminals. [FBrf0108310]
Joiner and Griffith, 1997, J. Neurosci. 17(23): 9384--9391
CaM kinase II and visual input modulate memory formation in the neuronal circuit controlling courtship conditioning. [FBrf0100089]
Griffith et al., 1994, Proc. Natl. Acad. Sci. U.S.A. 91(21): 10044--10048
Calcium/calmodulin-dependent protein kinase II and potassium channel subunit eag similarly affect plasticity in Drosophila. [FBrf0077243]
Levine et al., 1994, Neuron 13(4): 967--974
Altered circadian pacemaker functions and cyclic AMP rhythms in the Drosophila learning mutant dunce. [FBrf0077010]
Wang et al., 1994, Neuron 13(6): 1373--1384
Concomitant alterations of physiological and developmental plasticity in Drosophila CaM kinase II-inhibited synapses. [FBrf0077003]
Griffith et al., 1993, Neuron 10(3): 501--509
Inhibition of calcium/calmodulin-dependent protein kinase in Drosophila disrupts behavioral plasticity. [FBrf0059167]
Abstract
Griffith et al., 1991, Greenspan, Palka, 1991: 2
Functional studies of calcium/calmodulin-dependent protein kinase in learning and memory. [FBrf0078533]