Allele Dmel\brp⁶⁹

General Information
Symbol	Dmel\brp⁶⁹	Species	D. melanogaster
Name		FlyBase ID	FBal0194770
Feature type	allele	Associated gene	Dmel\brp

Map ( GBrowse )
Allele class
Mutagen	Delta2-3
Recent Updates
Description	What does this section display? This section contains items that were added to this record for each release. It currently only tracks new links between this FlyBase report and other FlyBase data classes (e.g. genes, references, stocks) or controlled vocabulary terms (e.g. GO, anatomy terms). What does this section not display? This section does not currently display links that were removed or gene model changes.
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FB2013_03
FB2013_02
All updates	Click here to see a list of all updates to this record from FB2010_08 and on.
Nature of the Allele
Allele class
Mutagen	Delta2-3 (Kittel et al., 2006)
Mutations Mapped to the Genome

Type Location Additional Notes References deletion 2R:5,403,428..5,428,122 comment=A deletion of brp sequences caused by mobilization of the P{SUPor-P}KG03268 and P{SUPor-P}brp[KG04653b] elements within the gene. (Fouquet et al., 2009)
Associated Sequence Data
DDBJ / EMBL / GenBank	DNA sequence Protein sequence Name

UniProtKB/Swiss-Prot
UniProtKB/TrEMBL

Progenitor genotype	P{SUPor-P}brp^KG04653b (Kittel et al., 2006) P{SUPor-P}KG03268 (Kittel et al., 2006)
Nature of the lesion	Statement Reference Transmobilization of elements P{SUPor-P}KG04653b and P{SUPor-P}KG03268 resulting in the deletion of most of the brp gene, leaving only the 5' regions, exon 1, exon 2 and part of exon 3. (Kittel et al., 2006)
Cytology
Phenotypic Data
Phenotypic Class
	lethal \| larval stage (with Df(2R)BSC29) (Kittel et al., 2006) neuroanatomy defective (with Df(2R)BSC29) (Kittel et al., 2006) neuroanatomy defective \| third instar larval stage (Fouquet et al., 2009) neurophysiology defective (with Df(2R)BSC29) (Kittel et al., 2006)
Phenotype Manifest In
	embryonic/larval neuromuscular junction (Kittel et al., 2006) embryonic/larval neuromuscular junction \| third instar larval stage (Fouquet et al., 2009) presynaptic cytoskeletal matrix assembled at active zones \| third instar larval stage (Fouquet et al., 2009) t-bar (Kittel et al., 2006)
Detailed Description
	Statement Reference T bars are missing at the active zones of the neuromuscular junction in mutant third instar larvae. (Fouquet et al., 2009) 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. (Kittel et al., 2006)
External Data
Linkouts
Interactions
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement Reference Heterozygosity for brp[69] results in a significant reduction in the increase in quantal content (QC) normally observed in homozygous Df(2R)KT40 mutant larvae. (Tsurudome et al., 2010)
Xenogenetic Interactions
Statement Reference
Complementation & Rescue Data
Rescued by	brp⁶⁹/Df(2R)BSC29 is rescued by Scer\GAL4^Rapgap1-OK6/brp^{D1-4.Scer\UAS.T:Avic\GFP-EGFP} (Fouquet et al., 2009)
Partially rescued by	brp⁶⁹/Df(2R)BSC29 is partially rescued by Scer\GAL4^elav-C155/brp^Scer\UAS.cWa (Kittel et al., 2006) brp⁶⁹/Df(2R)BSC29 is partially rescued by Scer\GAL4^Rapgap1-OK6/brp^Scer\UAS.cWa (Kittel et al., 2006)
Not rescued by	brp⁶⁹/Df(2R)BSC29 is not rescued by Scer\GAL4^Rapgap1-OK6/brp^{D1-3.Scer\UAS.T:Avic\GFP-EGFP} (Fouquet et al., 2009) brp⁶⁹/Df(2R)BSC29 is not rescued by Scer\GAL4^Rapgap1-OK6/brp^{D2-4.Scer\UAS.T:Avic\GFP-EGFP} (Fouquet et al., 2009)
Comments	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[69]/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[69]/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[69]/Df(2R)BSC29 third instar larvae, although small electron-dense aggregates are often seen localised to the active zone membrane. (Fouquet et al., 2009) Expression of the brp^Scer\UAS.cWa transgene, under the control of either Scer\GAL4^OK6 or Scer\GAL4^elav-C155, rescues the larval lethality of brp⁶⁹/Df(2R)BSC29 mutants. In addition, Scer\GAL4^OK6>brp^Scer\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. (Kittel et al., 2006)
Stocks ( 0 )

Notes on Origin
Discoverer

External Crossreferences & Linkouts
Other Crossreferences

Linkouts

Synonyms & Secondary IDs ( 2 )
Reported As
Symbol Synonym	brp⁶⁹ (Kittel et al., 2006, Kittel et al., 2006, Fouquet et al., 2009, Johnson et al., 2009, Owald et al., 2010) Brp⁶⁹ (Cheng et al., 2011)
Name Synonym
Secondary FlyBase IDs

References ( 7 )
Research paper	Cheng et al., 2011, J. Cell Biol. 194(6): 921--935 S6 kinase localizes to the presynaptic active zone and functions with PDK1 to control synapse development. [FBrf0216911] Owald et al., 2010, J. Cell Biol. 188(4): 565--579 A Syd-1 homologue regulates pre- and postsynaptic maturation in Drosophila. [FBrf0210057] Tsurudome et al., 2010, Neuron 68(5): 879--893 The Drosophila miR-310 Cluster Negatively Regulates Synaptic Strength at the Neuromuscular Junction. [FBrf0212495] Fouquet et al., 2009, J. Cell Biol. 186(1): 129--145 Maturation of active zone assembly by Drosophila Bruchpilot. [FBrf0208461] Johnson et al., 2009, PLoS Biol. 7(9): e1000193 Negative regulation of active zone assembly by a newly identified SR protein kinase. [FBrf0208771] Kittel et al., 2006, Science 312(5776): 1051--1054 Bruchpilot promotes active zone assembly, Ca2+ channel clustering, and vesicle release. [FBrf0190611]
Supplementary material	Kittel et al., 2006, Science 312(5776): Supporting online material for "Bruchpilot promotes active zone assembly, Ca[2+]-channel clustering, and vesicle release". [FBrf0199085]

Allele Dmel\brp69

Allele Dmel\brp⁶⁹