FB2025_01 , released February 20, 2025
Allele: Dmel\babo32
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General Information
Symbol
Dmel\babo32
Species
D. melanogaster
Name
FlyBase ID
FBal0094581
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

babo32 contains a deletion that removes the start codon and part of the extracellular domain.

Deletion removing part of the P{cp70ZT} and extending into the babo transcription unit up to base pair 850. The deletion removes the translation start site and the first 53 amino acids.

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

axon & photoreceptor cell

axon & photoreceptor cell R7 (with babo52)

axon & photoreceptor cell R8 (with babo52)

ganglion mother cell & larval optic lobe (with babo52)

photoreceptor cell R7 & axon (with babo52)

photoreceptor cell R8 & axon (with babo52)

Detailed Description
Statement
Reference

babo32 third instar larval C4da neurons do not show any obvious defects in the dendritic arborization, as compared to controls.

The transverse nerve makes ectopic connections at the neuromuscular junction in babo32/babo52 larvae.

Ectopic connections are formed at the neuromuscular junction in babo32/babo52 larvae.

babo32/babo52 animals pupariate in the food, show defects in anterior spiracle eversion (43%) and a significant incidence of bent legs at pharate stages (64%).

babo32/babo52 prepupae have a smaller brain lobe than normal and a reduced lamina plexus. Axon projections of the R7/R8 photoreceptor cells to the medulla are abnormal, with their growth cones forming bundles instead of the normal regular lattice network seen in controls. Photoreceptor axon targeting is still highly perturbed in 3 day old pupae and rotation of the medulla and lamina relative to one another does not take place. In the most strongly affected cases, babo32/babo52 mutants show a great reduction in the number of lamina cap and cartridge neurons. babo32/babo52 third instar larvae have a disorganised and smaller medulla neuropil compared to wild type. The number of glial cells at both the lamina and medulla is reduced in babo32/babo52 white prepupae compared to wild type.

The medulla neuropil is smaller than normal in babo26/babo32 white prepupae.

The optic lobe is much smaller than wild type in babo32/babo52 white prepupae. There is an approximately 50% decrease in the number of medial optic lobe neuroblasts compared to controls, a decrease in the number of ganglion mother cells produced from these medulla neuroblasts and a subsequent decrease in the number of maturing neurons within the medulla cortex. There is also a decrease in the number of lamina precursor cells and thus a decrease in the number of lamina cartridges and laminar neurons.

The number of cells in M phase in the developing optic lobes is significantly reduced in babo32/babo52 third instar larvae compared to controls. The size of the outer proliferation center and inner proliferation center zones is reduced in these larvae, although they still contain many cells in S phase. The ratio of M-phase cells to S-phase cells is thus reduced in the mutant optic lobes compared to wild type.

In babo32 mutant embryos, the ISNb and SNa branches enter the correct muscle fields but fail to extend correctly. In 24% of hemisegments, ISNb axons stall prematurely and in 20% of hemisegments the SNa fails to defasciculate resulting in loss of either dorsal or lateral branches.

Embryos derived from babo52 germline clones crossed to babo32 fathers show a greater penetrance of ISNb and SNa axon guidance defects compared to zygotic mutants.

Photoreceptor R1-R6 axons project into the brain and form a relatively normal but very reduced lamina in babo32/babo52 mutant larvae, but R7 and R8 axons never form a normal lattice network and their growth cones are collapsed. The medulla neuropil is significantly reduced in size and altered in morphology in babo32/babo52 mutant larvae.

100% of babo32/Df(2R)Np3 animals exhibit head capsule defects.

Homozygous larvae show slowed development, sort body and enlarged anal pads. Very few homozygotes progress to the pharate stage. Larvae do not leave food and do not evert their anterior spiracles. Adult structures of a babo52/babo32mutant derived from germ line clones are reduced in size. Axons from the developing eye project into the brain but do not find their targets. Brain hemispheres are reduced in size and show failure of active cell division, with no increase in cell death. Wing disc is reduced in size.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference

babo32 has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by daw[+]/daw3

Suppressed by
Statement
Reference

babo32/babo52 has abnormal neuroanatomy phenotype, suppressible by CycAC8LR1/CycA[+]

Enhancer of
Statement
Reference

babo[+]/babo32 is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of daw3

NOT Enhancer of
Statement
Reference

babo[+]/babo32 is a non-enhancer of visible | heat sensitive phenotype of peb1

NOT Suppressor of
Statement
Reference

babo[+]/babo32 is a non-suppressor of visible | heat sensitive phenotype of peb1

Phenotype Manifest In
Enhanced by
Statement
Reference

babo32 has larval intersegmental nerve phenotype, enhanceable by daw[+]/daw3

Suppressed by
Statement
Reference

babo32/babo52 has axon & eye photoreceptor cell phenotype, suppressible by CycAC8LR1/CycA[+]

babo32/babo52 has lamina phenotype, suppressible by CycAC8LR1/CycA[+]

Enhancer of
Statement
Reference

babo[+]/babo32 is an enhancer of larval intersegmental nerve phenotype of daw3

NOT Enhancer of
Statement
Reference

babo[+]/babo32 is a non-enhancer of eye | heat sensitive phenotype of peb1

NOT Suppressor of
Statement
Reference

babo[+]/babo32 is a non-suppressor of eye | heat sensitive phenotype of peb1

Other
Statement
Reference
Additional Comments
Genetic Interactions
Statement
Reference

The photoreceptor axon targeting and lamina neuron defects seen in babo32/babo52 mutants are substantially suppressed by CycAC8LR1/+.

In daw3/+; babo32/+; double mutant embryos, 20% of hemisegments show ISNb pathfinding defects as opposed to only 2% in daw3/+ single mutants and 4% in babo32/+ single mutants.

5% of babo32, ptcH84 double heterozygotes exhibit head capsule defects.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Separable from: a second mutation on the chromosome, which when homozygous leads to developmental delay and severely reduced cell proliferation.

Comments
Comments

Probably a null allele.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
References (19)