FB2024_03 , released June 25, 2024
Allele: Dmel\babo9
Open Close
General Information
Symbol
Dmel\babo9
Species
D. melanogaster
Name
FlyBase ID
FBal0144438
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Cytology
Description
Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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 ( 0 )
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

Unlike in wild type, where dendrites cluster around the photoreceptor axons in their cognate column, babo9 mutant Tm20 neuron clones extend their neurons laterally in medulla layer M3a and invade neighboring columns. Furthermore, the mutant dendritic branches in the internal medulla M8 layer exhibit a similar overextension phenotype. The mutant Tm20s' axons are correctly targeted to the fifth layer of the lobula.

The dendritic terminating frequency of babo9 mutant Tm20 neurons is significantly reduced compared to wild type, although the dendritic branching frequency was only mildly affected. The axonal locations and dendrite planar projection pattern of babo9 mutant Tm20 are comparable to those of wild type, while the percentage of dendritic branches terminating in medulla layer M3a is increased by approximately 12%.

babo9 mutant Tm20 neurons form aberrant synapses with neighbouring photoreceptors. babo9 mutant Tm20 dendrites contact the presynaptic sites of both cognate and neighboring rhabdomere R8s.

The dendrites of babo9 mutant Dm8 neuron clones occupy a larger space than wild type ones. babo9 mutant Dm8 dendrites occupy significantly more dendritic field units than the wild type ones. As in wild type, babo9 mutant Dm8 neurons are routed to medulla layer M6.

Homozygous clones in the larval optic lobe and central brain contain 30-50% fewer cells than wild-type control clones in similar positions.

A significant proportion of babo9 mosaic flies exhibit mutant R7 photoreceptor cells and do not phototax to visible light.

R7 photoreceptor clones homozygous for babo9 invade neighboring columns occupied by wild-type R7s.

babo9 mutant R7 photoreceptor cells target correctly at 40 hours after puparium formation (APF), but extend laterally into neighboring columns at 50 hours APF.

babo9 mutant dorsal cluster neuron clones display various anomalies. These defects include arrest of most axons at the protocerebrum---optic lobe junction, overextension of neurites from the ipsilateral lobular complex, ectopic projections in the central brain and aberrant fasciculation of processes. There is a delay in the initial development of babo9 mutant dorsal cluster neurons compared to wild-type neurons. There are no detectable babo9 dorsal cluster clones until 3 days after larval hatching, which is roughly one-half day late compared with wild-type neurons. babo9 clones undergo minimal morphogenesis during larval development and remain tiny. Misrouting of mutant neurites becomes evident by 24h APF. The mutant clones contain similar numbers of cell bodies to wild-type clones, suggesting that development of dorsal cluster neurons is delayed but not blocked. Single cell/two cell babo9 clones of dorsal cluster neurons fail to extend axons into the contralateral optic lobe and their initial trajectories can be kinky compared to wild-type clones. MARCM babo9 clones of ellipsoid body neurons are slow in initial morphogenesis. babo9 axons correctly navigate and initiate arborization inside the ellipsoid body but their arbors fail to converge properly at the midline, resulting in a deformed ellipsoid body ring. babo9 γ neuron clones show mushroom body defects.

When single cell mutant clones in adult γ neurons, abnormal projection patterns are seen. Mutant neurons possess two major axonal branches that project perpendicularly away from each other, as in larval γ projections. Wild-type patterns of dendrites and axons are seen in mutant γ neurons before puparium formation. However pruning of larval dendrites and axons does not happen to mutant neurons during early metamorphosis, persisting to adult stages. Mutant neuroblasts clones lack the prominent γ-lobe and instead possess the retained larval dorsal/ventral lobes in addition to the weak core α/β lobes.

Single cell mutant γ neuron MARCM clones in the mushroom body have abnormal dendritic arborisation patterns; 50% of mutant neurons have only one primary branch (wild-type neurons have 3 or more primary dendritic branches). Most mutant dendrites appear to originate within a narrow circumferential region above the equator of the adult calyx (whereas in wild type, secondary branching points are distributed widely over the primary neurites). In the wild-type, dendrites usually elaborate in a non-overlapping manner and their individual terminal branches occupy discrete territories. Wild-type dendrites from different clonal units are widely distributed and outline the entire calyx. In contrast, mutant dendrites derived from different clonal units often become extensively intermingled and occupy a relatively restricted space close to the central anterior surface of the calyx, forming an ectopic fourfold dendritic domain.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference
Suppressed by
NOT suppressed by
Enhancer of
Statement
Reference

babo9/babo[+] is an enhancer of mushroom body | somatic clone phenotype of SMC1LL01162

Additional Comments
Genetic Interactions
Statement
Reference

The axon pruning defects and reduction in clone size seen in homozygous SMC1LL01162 mushroom body clones are enhanced in a babo9/+ background.

Removing neighboring R7 photoreceptor cells through a sevV1 background greatly increases the tendency of babo9 mutant R7s to invade adjacent targets. Approximately 75% of isolated babo9 R7 terminals extend laterally into neighboring columns (as compared to 12.7% for babo9 mutants in a wild-type background).

The addition of EcRB1.Scer\UAS driven by Scer\GAL4Tab2-201Y partially rescues the gamma-lobe phenotype. The addition of EcRB2.Scer\UAS or EcRA.Scer\UAS driven by Scer\GAL4Tab2-201Y partially rescues the gamma-lobe phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Partially rescued by
Comments

Expression of baboa.Scer\UAS under the control of Scer\GAL4Act.PU, targeted to the Tm20 neurons using Ecol\lexADBD.Scer\UAS.T:Zzzz\ZipRREEL and Hsim\VP16C1a.AD.ort.T:Zzzz\ZipEERRL, rescues the dendritic phenotype seen in babo9 mutant Tm neuron clones.

Expression of baboa.Scer\UAS, under the control of Scer\GAL4Tab2-201Y, in babo9 mutant γ neurons fully rescues mushroom body remodeling defects. Scer\GAL4Tab2-201Y>baboa.Scer\UAS expression provides a significant but incomplete rescue of dorsal cluster neuron defects. Scer\GAL4Tab2-201Y>babob.Scer\UAS expression also provides a partial rescue of dorsal cluster neuron defects but fails to rescue γ neuron defects.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (9)