|Feature type||allele||Associated gene||Dmel\Acsl|
|Also Known As||dAcslKO|
|Allele class||loss of function allele|
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|Nature of the Allele|
|Mutations Mapped to the Genome|
|Associated Sequence Data|
|Nature of the lesion|
Recombination between the two progenitor insertions has resulted in the deletion of the sequence between them.
|Caused by aberration|
|Phenotype Manifest In|
Acsl[KO] is an early larval lethal allele. In the cross section of the larval segmental nerves of Acsl[KO]/Acsl mutants, there are conspicuous axonal swellings packed with heterogeneous membranous organelles. These aggregates, most often observed in posterior axons, include dark, prelysosomal and multivesicular bodies. In some mutant larvae, autophagosomes are also observed where a cluster of large clear-core vesicles are surrounded by a double-layer membrane. The mutant nerves also display lamellated bodies which resemble autolysosomes. In other cases, clusters of large clear-core vesicles are observed. These membrane aggregates are rarely found in wild-type axons. Acsl[KO]/Acsl mutants display pronounced dystrophy of larval neuromuscular junction 4 (NMJ4) in the posterior abdominal segments A6 and A7, while the muscle and larval size are comparable to wild-type. The bouton number and the synaptic area are significantly reduced in Acsl[KO]/Acsl mutants compared with wild-type. The synaptic area of Acsl[KO]/Acsl in Acsl[KO]/Acsl mutants is comparable to that of wild-types 2 days after egg laying (AEL). Synapse growth during 2-3.5 days AEL of Acsl[KO]/Acsl mutants is markedly slower than that in wild-types. From 3.5 to 5 days AEL, the mutant NMJ synapses apparently retract. The evoked excitatory junction potentials (EJPs) are significantly reduced in Acsl[KO]/Acsl mutant larvae recorded from muscle 6 in the posterior abdominal segment. Miniature EJPs (mEJPs, also known as quantal size) are normal in Acsl[KO]/Acsl mutants. Quantal content is significantly reduced in Acsl[KO]/Acsl mutants.
Acsl05847/AcslKO has neuroanatomy defective | larval stage phenotype, suppressible by Hsap\ACSL4Scer\UAS.L.T:Hsap\MYC/Scer\GAL4αTub84B.PL
Acsl05847/AcslKO has neurophysiology defective phenotype, suppressible | partially by Scer\GAL4Mhc.PW/Hsap\ACSL4Scer\UAS.L.T:Hsap\MYC
Acsl05847/AcslKO has neurophysiology defective phenotype, suppressible by Hsap\ACSL4Scer\UAS.L.T:Hsap\MYC/Scer\GAL4αTub84B.PL
|Phenotype Manifest In|
Acsl05847/AcslKO has bouton phenotype, suppressible by Scer\GAL4elav.PU/Hsap\ACSL4Scer\UAS.L.T:Hsap\MYC
|NOT suppressed by|
Expression of Hsap\ACSL4[Scer\UAS.L.T:Hsap\MYC] in postsynaptic muscles driven by Scer\GAL4[Mhc.PW] does not suppress the dystrophic neuromuscular junctions of Acsl[KO]/Acsl mutants for bouton number. Neuronal expression of Hsap\ACSL4[Scer\UAS.L.T:Hsap\MYC] at 2.5 days after egg laying (AEL) fully suppresses the reduced synaptic area phenotype of Acsl[KO]/Acsl mutants. Neuronal expression of Hsap\ACSL4[Scer\UAS.L.T:Hsap\MYC] driven by Scer\GAL4[elav.PU] restores the bouton number to wild-type levels in Acsl[KO]/Acsl mutants. The neuromuscular junction phenotypes of Acsl[KO]/Acsl mutants can be fully suppressed by ubiquitous expression of Hsap\ACSL4[Scer\UAS.L.T:Hsap\MYC] under the control of Scer\GAL4[αTub84B.PL]. The reduced EJPs and quantal content are fully rescued by Hsap\ACSL4[Scer\UAS.L.T:Hsap\MYC] expressed in either ubiquitously via Scer\GAL4[αTub84B.PL] or pan-neuronally via Scer\GAL4[elav.PU]. EJPs in animals with Hsap\ACSL4[Scer\UAS.L.T:Hsap\MYC] expressed pan-neuronally are mildly but significantly higher than that in wild-types. Postsynaptic expression of Hsap\ACSL4[Scer\UAS.L.T:Hsap\MYC] driven by Scer\GAL4[Mhc.PW] in Acsl[KO]/Acsl mutant background slightly suppressed the EJP phenotype.
|Complementation & Rescue Data|
|Stocks ( 1 )|
|Notes on Origin|
|External Crossreferences & Linkouts|
|Synonyms & Secondary IDs ( 2 )|
|Secondary FlyBase IDs|
|References ( 3 )|
|Personal communication to FlyBase|