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General Information
Symbol
Dmel\amx1
Species
D. melanogaster
Name
FlyBase ID
FBal0000504
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
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 )
 
Disease-implicated variant(s)
 
Phenotypic Data
Phenotypic Class
Phenotype Manifest In
Detailed Description
Statement
Reference

Embryos laid by amx1/Df(1)Exel9049 mutant females exhibit a strong neurogenic phenotype with a dramatic increase in the number of neurons and fail to hatch, resulting in female sterility.

Stage 8 embryos produced from homozygous amx1 mutant mothers contain an increased number of neuroblasts compared to wild type. More than 90% of embryos are neurogenic and ~10% have denticles.

Embryos from amx1/Df(1)10-70d females die and show the hypertrophy of the central nervous system characteristic of amx1/amx1 progeny.

Displays locomotor activity rhythm with an approximately 24h period.

Hyperplasia of replicating sensory precursors: due to an increased number of ectodermal cells being recruited as sensory precursor cells.

amx1 shows neural hypertrophy, a 2-5 fold increase in nau expressing cells per cluster relative to wild type.

Increase in SMCs per cluster in embryos lacking the maternal product.

Variable embryonic neurogenic phenotype.

Most homozygotes are indistinguishable from wild-type, but some flies have smaller eyes than normal with disarranged facets, giving a rough eye phenotype.

Eyes slightly reduced, narrower below; trident pattern stronger than in lz. Studies by Shannon (FBrf0023892) show that amx1 progeny and many amx1/+ progeny of amx1 mothers are embryonic lethals. Ovaries and egg production of amx1 females normal. General disorganization of early embryo with amx1/+ progeny of amx1 mothers less extreme than amx1 progeny (FBrf0025447) amx1/+ daughters show 0.2% survival; amx1/Dp(1;1)lz-2 show considerably higher survival (FBrf0040181); Lethal embryos exhibit hypertrophy of central nervous system at the expense of epidermal tissue (FBrf0037306; FBrf0040185). Similarly peripheral nervous elements, the sensilla, exhibit increased numbers and abnormal morphology; cells diverted from epidermal to neurological pathway (FBrf0045357). Embryonic phenotype locally rescuable by injections of ooplasm from wild-type or pcxunspecified ova during preblastoderm stages (FBrf0040181; FBrf0042361). lz/amx1 is wild type. Mosaics in amx1/+ daughters of +/+ or amx1/+ females show that ventral tissues are sensitive to reduced amx+ activity; no clones of amx1 tissue found in cuticle of amx1/+ daughters of amx1 mothers (FBrf0041016). RK2.

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

The heat-shocked progeny from heterozygous amx1 females crossed to N3.hs.T:Scer\GAL4,T:Hsim\VP16 males hatch at a similar rate to wild type and are viable.

The heat-shocked progeny from heterozygous amx1 females crossed to NECN.3.hs.T:Scer\GAL4,T:Hsim\VP16 males hatch at a similar rate to wild type and are viable.

The heat-shocked progeny from heterozygous amx1 females crossed to Nicd.hs males hatch at a reduced rate compared to wild type and only around 50% reach adulthood.

The neurogenic phenotypes seen in stage 8 embryos when homozygous amx1 mutant females are crossed to N3.hs.T:Scer\GAL4,T:Hsim\VP16 males (heat-shocked before the first delamination round) are similar to those seen when amx1 females are crossed to wild type males.

The neurogenic phenotypes seen in stage 8 embryos when homozygous amx1 mutant females are crossed to NΔECD.hs.cUa males (heat-shocked before the first delamination round) are similar to those seen when amx1 females are crossed to wild type males.

Fewer neurogenic phenotypes are seen in stage 8 embryos when homozygous amx1 mutant females are crossed to Nicd.hs males (heat-shocked before the first delamination round) than when amx1 females are crossed to wild type males.

No effect on the faf eye phenotype.

Xenogenetic Interactions
Statement
Reference

The sterility of amx1/Df(1)Exel9049 mutant females and the neurogenic phenotype seen in the progeny (the embryos contain dramatically increased number of neurons and fail to hatch) is partially rescued by combination with Hsap\TM2D3amx.1 (some of the embryos show a complete rescue of the neurogenic phenotype and the hatching rate reaches almost 35%), whereas Hsap\TM2D3P155L.amx fails to improve the phenotypes.

Complementation and Rescue Data
Partially rescued by
Not rescued by
Comments

amx+t3.325 fully rescues the sterility of amx1/Df(1)Exel9049 mutant females and the neurogenic phenotype seen in the progeny (the embryos contain dramatically increased number of neurons and fail to hatch).

Expression of amxScer\UAS.cMa under the control of Scer\GAL4arm.PU partially rescues the neurogenic cuticle phenotypes seen in embryos derived from amx1 mutant females. Approximately 80% of embryos are neurogenic and ~40% have denticles.

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Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (2)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (24)