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General Information
Symbol
Dmel\abd-AMX1
Species
D. melanogaster
Name
FlyBase ID
FBal0000083
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
abdAMX1
Key Links
Mutagen
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

Mutations in the transcription unit.

Lesion mapped to: 54-56 kb.

Caused by aberration
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

gonad & parasegment 10

gonad & parasegment 11

gonad & parasegment 12

Detailed Description
Statement
Reference

abd-AMX1 mutant embryos show a significant increase in the proportion of mitotic neuroblast daughter cells, but not of mitotic neuroblasts, only in the A5 ventral nerve cord segment, as compared to controls.

abd-AMX1 embryos show reduced heart lumen size, reduced ostia cell size and ostia cells are rounder, losing their characteristic elongated shape.

Abdominal hemisegments of abd-AMX1 mutant embryos do not show an increase in glial progeny, but generate ectopic neurons in the dorsal lateral cortex owing to homeotic transformation of NB6-4a to NB6-4t (in 100% of hemisegments).

abd-AMX1 mutants are still able to form seven pairs of alary muscles along the cardiac tube, as in wild-type.

NB6-4a-to-NB6-4t neuroblast homeotic transformations occur in abd-AMX1 mutants.

Stage 15 abd-AMX1 embryos have only ~18 genital disc precursor cells, instead of the wild-type number of 22.

Male-specific somatic gonadal precursors are present in male abd-AMX1 mutant stage 13 embryos, while somatic gonadal precursors do not develop in parasegment 10-12.

In mutant embryos, the width of the heart is now the same as that of the aorta when compared with the wild-type. Also the expression pattern of markers suggest that heart cardioblasts have not been specified in the posterior of the dorsal vessel and these posterior cardioblasts have been transformed instead into aorta cardioblasts.

Homozygous embryos show no heart formation and lack dorsal closure.

Failure of somatic gonadal precursor (SGP) specification in mutants.

Germ cells are able to move through the posterior midgut and initially find lateral mesoderm. The germ cells fail to maintain their specific association with the mesoderm and disperse in the posterior of the embryo. Gonadal mesoderm fails to develop.

abd-Aiab3-Uab4/abd-AMX1 larvae have approximately 12 postembryonic neuroblasts in each of the abdominal neuromeres A3 to A7 (compared to 6 in wild-type). Each of these extra neuromeres produces a hundred or more progeny.

Ectopic fat body precursors arise in parasegments 10-12: transformation of somatic gonadal precursor (SGP) cells into primary fat body clusters.

First instar larvae exhibit lateral dots (a paired structure found in A1 segment of wild type) in abdominal segment A2 to A5 and rarely in A6.

Hemizygous embryonic phenotype displays complete transformation of abdominal parasegments 7, 8 and 9 into parasegment 6 and partial transformation of abdominal parasegments 10 to 13 into parasegment 6 (FBrf0043314).

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

abd-AMX1 Df(3R)Ubx109 double mutant embryos show a large reduction in alary muscle number, with only occasional muscles observed. Of the few muscles that develop, all were randomly positioned and are not true alary muscle pairs.

The homeotic transformation of NB6-4a to NB6-4t, observed in abd-AMX1 mutants is suppressed in CycEAR95 mutants.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer

Morata.

J. Casanova.

Comments
Comments

The A and B glial cells do not show a pattern defect.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (5)
References (32)