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General Information
Symbol
Dmel\mam9
Species
D. melanogaster
Name
FlyBase ID
FBal0012017
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
mamIL42
Key Links
Allele class
Nature of the Allele
Allele class
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Nucleotide change:

C14056539T

Amino acid change:

Q1159term | mam-PA; Q1159term | mam-PB; Q1159term | mam-PD

Reported amino acid change:

Q1038term

Comment:

Position of mutation on reference sequence inferred by FlyBase curator.

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

Amino acid replacement: Q1038term.

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

Mutant embryos have a strong loss of asymmetry phenotype with GMC-1 of the RP2/sib lineage dividing symmetrically into two RP2 neurons in as many as 80% of hemisegments, resulting in a duplication of RP2 neurons.

Embryonic CNS exhibits severe disturbances and larval exhibit weak cuticle loss.

Weak embryonic neurogenic phenotype.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Both the daughter cells of the GMC-1 of the RP2/sib lineage adopt an RP2 fate in mam9 numb796 double mutant embryos, indicating that mam is epistatic to numb.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Not rescued by
Comments

The loss of asymmetric division in GMC-1 of the RP2/sib lineage and the neurogenic phenotype seen in mam9 embryos is not rescued by expression of mamN.Scer\UAS under the control of Scer\GAL4hs.PH between 6 and 8 hours of development. mam44 and mam9 show interallelic complementation; there is a significant rescue of the loss of asymmetric division in GMC-1 of the RP2/sib lineage, so that most hemisegments show normal specification of the RP2sib neuron in transheterozygotes.

Images (0)
Mutant
Wild-type
Stocks (0)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (5)