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General Information
Symbol
Dmel\comm1
Species
D. melanogaster
Name
FlyBase ID
FBal0030916
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Comment:

comm1 is a deletion of 9bp with an insertion of 2bp, causing a frameshift at amino acid 217. This leads to premature translation termination after the addtion of 26 novel amino acids. The annotated deletion endpoints are approximate.

Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

Frameshift mutation at amino acid 217, resulting in a premature termination following 26 amino acids of the novel reading frame.

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

Commissural axons are prevented from forming in comm1 mutants.

Mitotically recombined neuronal clones homozygous for comm1 cross the ventral midline in 70% of cases, compared to 85% of cases in wild-type samples.

The commissures form in 21.9% of mutant embryos, although commissure formation is usually restricted to one or two thoracic segments.

The commissures are almost all absent in homozygous embryos, with axons only crossing the midline in about 9% of embryos.

All commissural axons fail to cross the midline.

comm1 mutants have a commissureless phenotype.

The motoneuron growth cones fail to initiate synaptogenesis on contacting their target muscles in homozygous or comm1/comm5 embryos. The axons either stall just short of synaptic targets or they extend beyond the normal stopping points without apparently settling on alternative targets. These phenotypes are seen in the five motoneuron nerve groups (the ISN, SNa, SNb, SNc and SNd).

Strong allele. Commissures are not completely absent but partial and highly abnormal commissures form. Rare adult escapers of hypomorphic allelic combinations show a range of uncoordinated behaviors.

Commissural axons rarely cross the midline of the VNC, so the midline glia have minimal contact with axons. Temporal pattern of midline glial death correlates with a 39% decrease in numbers from stage 13 to stage 17 of embryogenesis, relative to a 21% decrease over the same period for wild type.

All commissural pathways are lacking, while other axon pathways appear normal. Differentiation of the brain commissure, involving the projection of many axons across the midline and formation of additional commissural fascicles, does not take place. As a result the brain commissure is greatly reduced.

Commissural axon pathways in the embryonic ventral nerve cord absent.

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

Using Scer\GAL4ftz.ng, expression of AblScer\UAS.cHa in a subset of neurons in a comm1 background causes a few thin commissures to reform.

Pan-neural expression of AblScer\UAS.cHa under the control of Scer\GAL4elav.PLu partially suppresses the comm1 commissure phenotype.

Pan-neural expression of AblKN.Scer\UAS under the control of Scer\GAL4elav.PLu partially suppresses the comm1 commissure phenotype.

Expression of AblKN.Scer\UAS in a subset of neurons under the control of Scer\GAL4ftz.ng partially suppresses the comm1 commissure phenotype.

The addition of learobo2-5 to comm1 embryos has no effect on the number of commissures crossing the midline in the ventral nerve cords in these mutants. The addition of comm1 to robo1, learobo2-5 embryos has no effect on the ventral nerve cord phenotype.

Xenogenetic Interactions
Statement
Reference

Pan-neural expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS under the control of Scer\GAL4elav.PLu partially suppresses the comm1 commissure phenotype.

Expression of Abl::Hsap\ABL1::Hsap\BCRP210.Scer\UAS in a subset of neurons under the control of Scer\GAL4ftz.ng partially suppresses the comm1 commissure phenotype.

Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4ftz.ng in comm1 embryos results in 49% of embryos showing some axons crossing the midline and in many cases thin commissures are present. Expression of Ggal\MLCKct.Scer\UAS under the control of Scer\GAL4elav.PLu in comm1 embryos results in partial commissure formation in 71% of embryos.

Complementation and Rescue Data
Partially rescued by
Comments
Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Symbol Synonym
Name Synonyms
Secondary FlyBase IDs
    References (12)