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General Information
Symbol
Dmel\beat-Ia3
Species
D. melanogaster
Name
FlyBase ID
FBal0057747
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
beat3
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference
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 )
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

beat-Ia3/beat-IaC163 third instar larvae often lack neuromuscular junctions (NMJs) on dorsal muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 1 (31%), muscle 9 (34%), muscle 2 (8%), muscle 10 (13%).

beat-Ia3/beat-IaC163 third instar larvae often lack neuromuscular junctions (NMJs) on ventral muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 12 (25%), muscle 13 (34%), muscle 6 (38%), muscle 7 (55%).

Cells of the Bolwig's organs (BOs) form in homozygous embryos, but the morphology of the larval visual system (LVS) is severely disrupted and increased numbers of photoreceptor cells are apparent from the earliest stages of LVS development. Extra photoreceptor cells are seen both in the normal location of the BO clusters and dispersed between the two clusters. Embryos sometimes contain three BO's and, rarely, four BO clusters are seen. Migration of the BOs appears relatively normal in some embryos, but in others it is disrupted and the BO does not achieve its proper location even though head involution appears normal, or the BO is elongated.

Motor axons exit the CNS normally but then fail to branch and enter their muscle domains once in the periphery. The SNb fails to diverge from the ISN either completely (full bypass), 45% segments, or partially (partial bypass), 39% segments, the SNc fails to diverge in 77% segments.

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

eveΔRP2A, beat-Ia[+], eve[+], beat-Ia3 is an enhancer of neuroanatomy defective phenotype of unc-58

unc-5[+], beat-Ia[+], unc-58, beat-Ia3 is an enhancer of neuroanatomy defective phenotype of eveΔRP2A

Suppressor of
Other
Statement
Reference
Phenotype Manifest In
NOT Enhanced by
NOT suppressed by
Statement
Reference

beat-IaC163/beat-Ia3, unc-58 has motor neuron phenotype, non-suppressible by Nrgl10

Enhancer of
Statement
Reference

eveΔRP2A, beat-Ia[+], eve[+], beat-Ia3 is an enhancer of intersegmental nerve phenotype of unc-58

unc-5[+], beat-Ia[+], unc-58, beat-Ia3 is an enhancer of intersegmental nerve phenotype of eveΔRP2A

Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference

Nrgl10/Y; beat-IaC163/beat-Ia3 double mutants exhibit intersegmental nerve axon stalling prior to the first branch point.

unc-58, beat-IaC163/beat-Ia3 double mutants exhibit intersegmental nerve axon stalling prior to the first branch point.

Nrgl10/Y; unc-58, beat-IaC163/beat-Ia3 triple mutants exhibit severe defects in the intersegmental nerve crossing in the ventral muscle field.

Nrgl10/Y; beat-IaC163/beat-Ia3 double mutants do not exhibit any aCC or RP2 exit phenotypes.

unc-58, beat-IaC163/beat-Ia3 mutants exhibit a failure of motor neurons to exit the CNS in 10% of hemisegments.

The addition of a Nrgl10/Y background does not affect the unc-58, beat-IaC163/beat-Ia3 CNS exit failure seen in 10% of unc-58, beat-IaC163/beat-Ia3 hemisegments.

A transheterozygous combination of eveΔRP2A/+, unc-58/+ reduces beat-Ia levels to 50% and significantly increases the defects seen in intersegmental nerves, with the number of axons that exhibit stalling increasing from 3% to 7.5% in eveΔRP2A/+, unc-58/+ transheterozygotes and eveΔRP2A/+, unc-58/+, beat-Ia3/+ triple heterozygotes, respectively.

CNS exit from EW neurons misexpressing eveScer\UAS.cBa is partially suppressed in an unc-58 beat-IaC163/beat-Ia3 mutant background while midline crossing is partially restored (in 15% of hemisegments).

The neuromuscular junction innervation defects seen in the dorsal muscles of beat-Ia3/beat-IaC163 third instar larvae are not enhanced by expression of sideScer\UAS.cSa under the control of either Scer\GAL4how-24B or Scer\GAL4Mef2.PR.

beat-Ia/+, SoxNGA1192/+ double heterozygous embryos commissures are partially fused and the longitudinal connectives are thinner or missing. This phenotype is not seen in either beat-Ia/+ or SoxNGA1192/+ embryos.

beat-Ia2/beat-Ia3 Rac1N17.Scer\UAS Scer\GAL4elav-C155 double mutant embryos exhibit additive, not synergistic effects on the ISNb full bypass phenotype.

In beat-Ia2/beat-Ia3 transheterozygotes the SNb fails to diverge from the ISN completely (full bypass) in 38% segments or partially (partial bypass) in 28% segments. The SNb divergence defect can be suppressed by Fas2e76 and the SNc defect by ConFvex238.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
References (9)