|Feature type||allele||Associated gene||Dmel\brp|
|Map ( GBrowse )|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
|Phenotype Manifest In|
T bars are missing at the active zones of the neuromuscular junction in mutant third instar larvae.
brp69/Df(2R)BSC29 mutants have slightly smaller NMJs and fewer individual synapses than wild-type larvae. However, individual receptor fields are enlarged in the mutants. In the mutant NMJs, postsynaptic densities appear larger than in wild type and there are intermittent rufflings of the presynaptic membrane. Notably, the brp69/Df(2R)BSC29 NMJs completely lack T-bars, but occasionally show a little residual electron-dense material attached to the active zone membrane. The average miniature excitatory junctional currents (mEJC) amplitude is increased in brp69/Df(2R)BSC29 mutants, while the frequency is not significantly altered. Quantal content of mutant NMJs is significantly decreased compared to controls. Although the rise time of eEJCs is significantly increased at mutant NMJs, the rise time of mEJCs is the same as controls. The decay time constant of eEJCs is not significantly altered at brp69/Df(2R)BSC29 synapses, while the decay time constant of mEJCs decay is longer in the mutant than in the control. A 10Hz stimulation of NMJs reveals transient short term facilitation of brp69/Df(2R)BSC29 currents and the absence of a frequency-dependent depression of steady-state current amplitudes compared with controls. Paired-pulse protocols applied to the NMJ do not produce marked facilitation at control synapses, while there is a prominent facilitation at mutant NMJs, showing that vesicle release at brp69/Df(2R)BSC29 synapses benefits from accumulation of Ca2+. After bath application of membrane-permeable EGTA-AM, the reduction of evoked vesicle release is more pronounced in mutants than in wild type. Additionally, there are a reduced number of Ca2+ channels over the entire NMJ and at synapses in brp69/Df(2R)BSC29 mutants compared to controls. These observations suggest that impaired vesicle release in the mutants is caused by mislocalization of presynaptic Ca2+ channels.
|Phenotype Manifest In|
|Complementation & Rescue Data|
|Partially rescued by|
|Not rescued by|
Expression of brp[D1-3.Scer\UAS.T:Avic\GFP-EGFP] under the control of Scer\GAL4[Rapgap1-OK6] fails to rescue the formation of T bars at the neuromuscular junction in brp/Df(2R)BSC29 third instar larvae. Expression of brp[D1-4.Scer\UAS.T:Avic\GFP-EGFP] under the control of Scer\GAL4[Rapgap1-OK6] rescues the formation of T bars at the neuromuscular junction in brp/Df(2R)BSC29 third instar larvae. Expression of brp[D2-4.Scer\UAS.T:Avic\GFP-EGFP] under the control of Scer\GAL4[Rapgap1-OK6] fails to rescue the formation of T bars at the neuromuscular junction in brp/Df(2R)BSC29 third instar larvae, although small electron-dense aggregates are often seen localised to the active zone membrane.
Expression of the brpScer\UAS.cWa transgene, under the control of either Scer\GAL4OK6 or Scer\GAL4elav-C155, rescues the larval lethality of brp69/Df(2R)BSC29 mutants. In addition, Scer\GAL4OK6>brpScer\UAS.cWa expression partially restores the lack of T-bars seen in these mutants, although T-bars in the rescued flies are somewhat aberrant in shape. Expression of the transgene with both drivers can partially rescue the drop in current amplitude from brp69/Df(2R)BSC29 NMJs.
|Stocks ( 0 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 2 )|
|Secondary FlyBase IDs|
|References ( 7 )|