FB2026_02 , released June 18, 2026
FB2026_02 , released June 18, 2026
Allele: Dmel\Mad1-2
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General Information
Symbol
Dmel\Mad1-2
Species
D. melanogaster
Name
FlyBase ID
FBal0052185
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Mad1.2, mad12
Key Links
Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

A 5013bp fragment of the P{lacW} transposon is inserted in the first intron of Mad.

Imprecise excision: P{lacW} sequences are retained at the site of the original insertion.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Variant Molecular Consequences
Associated Sequence Data
DNA sequence
Protein sequence
 
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

Mad1-2/Df(2L)C28 mutants show a significant reduction in bouton number at muscles 6/7 and 4 NMJs compared to controls.

R8 photoreceptor differentiation is normal in somatic clones of Mad1-2 mutant cells.

Eye differentiation (as marked by the presence of developing photoreceptors) fails in homozygous clones that touch the posterior margin of the eye disc.

Homozygous clones induced during the first larval instar stage cause a transformation of ommatidia into frons cuticle.

Class II allele. Eye discs are very small. Larval survival rate of homozygotes is 35% of heterozygotes with wild type. Morphogenetic furrow and photoreceptor differentiation are limited to the dorsal region of the disc. Resulting eyes are reduced along the dorsal-ventral axis. Cells do survive in clones. Clones located within the eye field proper show no effect on furrow propagation or eye development in general. Clones at the posterior eye margin cause failure of morphogenetic furrow initiation and pattern duplications. Double mutant clones of Mad1-2 with Pka-C1k08918 located in posterior locations show a phenotype similar to Mad single mutant clones, except that they are more frequently associated with overgrowth. Double mutant clones in more anterior positions show a novel phenotype, and are always associated with overgrowth with no ectopic furrow or photoreceptor differentiation. These clones give rise to head cuticle in adult flies.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhancer of
Statement
Reference
Suppressor of
Statement
Reference

Mad[+]/Mad1-2 is a suppressor of visible phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

Other
Phenotype Manifest In
Suppressed by
Enhancer of
Statement
Reference

Mad1-2 is an enhancer of photoreceptor cell R8 & eye disc | somatic clone phenotype of smo3

Suppressor of
Statement
Reference

Mad[+]/Mad1-2 is a suppressor | partially of terminal bouton phenotype of emaf07675

Mad[+]/Mad1-2 is a suppressor of wing vein | ectopic phenotype of Scer\GAL4Tub.PU, cswN308D.UASp

Other
Statement
Reference

Mad1-2, Su(H)del47, ci94 has photoreceptor cell R8 & eye disc | somatic clone phenotype

Mad1-2, ci94 has photoreceptor cell R8 & eye disc | somatic clone phenotype

Additional Comments
Genetic Interactions
Statement
Reference

myd3PM71/+, Mad1-2/+ double heterozygotes show a decrease in flight ability.

Mad1-2/+ partially suppresses the synaptic bouton number phenotype of homozygous emaf07675 mutants.

Eye disc cells simultaneously mutant for Mad1-2, ci94 and Su(H)del47 arrest in G1 after a severe delay but they never enter the second mitotic wave.

Cells mutant for Mad1-2 and Su(H)del47 do not enter the second mitotic wave, while cell cycle entry does occur in cells mutant for Mad1-2 and ci94.

R8 photoreceptor differentiation is delayed in ci94; Mad1-2 double mutant clones, and fails in ci94; Mad1-2; Su(H)del47 triple mutant clones. This is despite normal R8 differentiation in any of the single mutants (although sometimes early in Su(H)del47 single mutant clones), and in Mad1-2; Su(H)del47 double mutants.

Eye differentiation is rescued in Mad1-2 clones by eyaScer\UAS.cBa expressed under the control of Scer\GAL4dpp.blk1. smo3 Mad1-2 double mutant clones in the eye never develop photoreceptors whether they lie at the margin or in the interior of the eye disc. Occasionally an ommatidium forms along the edge of the clone, such that some of the component photoreceptors lie within the clone.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (5)
Notes on Origin
Discoverer

Separable from: Pka-C13UTR.

The Mad1-2 stock contained second-site mutations in Pka-C1; these mutations are represented by the Pka-C13UTR allele, and a Mad-mutant chromosome in which the second-site Pka-C1 mutations have been removed is referred to as 'Mad[1-2a]'.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (6)
References (42)