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General Information
Symbol
Dmel\lola5D2
Species
D. melanogaster
Name
FlyBase ID
FBal0039617
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Allele class
Nature of the Allele
Allele class
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
Insertion components
P{lacW}lola5D2
Product class / Tool use(s)
Encoded product / tool
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

axon & adult antennal lobe projection neuron | somatic clone

dendrite & adult antennal lobe projection neuron | somatic clone

Detailed Description
Statement
Reference

Females containing homozygous germline clones show defects in stage 14 egg chambers, including dumpless egg chambers (egg chambers in which the nurse cells have failed to transfer their cytoplasmic contents to the oocyte, have intact nuclei and do not appear to be undergoing programmed cell death) and egg chambers with persisting nurse cell nuclei (egg chambers in which nurse cells have transferred their cytoplasmic contents to the oocyte, but their nuclei have failed to undergo programmed cell death including nuclear condensation).

In mutant embryos, the motor axons that project through the SNb peripheral nerve fail to form connections to their cognate muscles. Most commonly, SNb axons appear to "stall" somewhere between the point at which they would normally separate from the ISN and the muscle 6/13 junction. In other hemisegments, SNb axons project through the muscles field but fail to branch into the intermuscle clefts where synapses should be formed. The phenotype is slightly stronger than seen in lola1A4.

In the embryonic CNS, longitudinal connectives are interrupted and commissures fuse. In some segments the VUM neurons are born and differentiate, but fail to form a well-defined posterior root to the anterior peripheral fascicle. Intersegmental nerve shows various aberrations, failing to grow or wandering into adjacent segments, or defasciculation of ISN sensory axons. The lateral chordotonal organs are sometimes displaced dorsally from their wild type position. There is no segment specificity of these phenotypes.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Enhancer of
Statement
Reference

lola5D2/lola[+] is an enhancer of wing margin phenotype of ct53d

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

Transposase induced excision of the P element reverts both the lethality and the mutant neuronal phenotype. The ISN phenotype and the lateral chordotonal organ phenotype shows incomplete expressivity. The trachea appear normal in the mutant embryos. The number of PNS neurons, their distribution into neuronal subtypes and differentiation appear normal.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (10)