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General Information
Symbol
Dmel\gcm1
Species
D. melanogaster
Name
FlyBase ID
FBal0045761
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
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

Excision of the P{PZ} insertion causes partial deletion of the P{PZ} element and flanking genomic DNA.

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

Although the structure of the nervous system is disrupted in mutant embryos and the dendritic arbors are abnormal, they continue to form in their characteristic locations and the fundamental distinction between ISN and SN motor dendritic fields is maintained.

Axonal elongations of the MP1/dMP2 and vMP2 neurons show no obvious abnormality in stage 13 gcmP/gcm1 embryos even though most of the misdifferentiated glial cells do not contact these longitudinal pioneer axons. Fasciculation of the MP1/dMP2 and vMP2 axons occurs normally in the absence of glial cells, although elongation is delayed and the fascicle looks thinner in some hemisegments. The dMP2 neurons send out axons in an abnormal orientation in some hemisegments of gcm1 embryos, occasionally joining with a motor pathway. The pCC pathway is broken or becomes thinner at stage 15. EG glial cells and peripheral glia are missing in stage 16 mutant embryos. The intersegmental and segmental nerves are separated and do not meet at the exit junction in mutant embryos (in contrast to wild type). The segmental nerve exits the CNS at a more ventral position than normal. Axon bundle formation is also affected in the peripheral nervous system. The ISNb motor axon apparently innervates target muscles, however the position of the muscles is sometimes abnormal.

Homozygous embryos exhibit severe axonal defects, longitudinal tracts have fewer axons than normal and the transverse commissures are sometimes fuzzy. There are few glial cells as they are transformed into neurons of the PNS. CNS neuromere remains elongated at the end of embryonic development, a condensation defect. Pioneer neurons can find their correct pathway without the help of glial cells.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (4)