FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\MadB1
Open Close
General Information
Symbol
Dmel\MadB1
Species
D. melanogaster
Name
FlyBase ID
FBal0052174
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
Progenitor genotype
Associated Insertion(s)
Cytology
Description

Insertion of P{lacW} into the first intron of Mad.

Allele components
Component
Use(s)
Inserted element
Encoded product / tool
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

MadB1/Mad12 clones in the wing pouch area of the wing disc have very poor survival rates.

When homozygous clones are made in the eye disc, furrow initiation is blocked in posterior margin cells of the eye disc.

Homozygous germ line clones (either germ line stem cells or spermatocytes) are generated in the testis, but they do not persist to the same extent as wild-type control clones.

Homozygous clones in the posterior of the eye disc do not appear to reorient the morphogenetic furrow in adjacent cells.

20% of the dorsal branch fusion events are disrupted. The fusion cell extends a sprout but does not contact the appropriate fusion partner.

Homozygous clones at the posterior margin of the eye disc fail to differentiate as photoreceptors, and often have a non-autonomous inhibitory effect on photoreceptor differentiation in surrounding wild-type cells.

Class I allele. Homozygous larvae survive to the late 3rd instar larval stage and lack imaginal discs. Larval fat body and the optic lobes of the CNS are dramatically reduced. Anterior midgut formation is abnormal. Larval survival rate of homozygotes is 25% of heterozygotes with wild type. Clonal analysis revealed that Mad function is autonomously required in the eye imaginal disc cells for proliferation and/or survival.

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

MadB1 is an enhancer of eye phenotype of scahs.roE

NOT Enhancer of
Statement
Reference

MadB1 is a non-enhancer of | heat sensitive phenotype of Chc1

Suppressor of
Statement
Reference

MadB1 is a suppressor of eye phenotype of tkvQ253D.GMR

Other
Additional Comments
Genetic Interactions
Statement
Reference

brkXH/brkXH, MadB1/Mad12 double mutant wing disc clones have normal apical-basal cell length.

As MadB1 clones in the wing pouch do not survive, and bskflp147E single mutant clones show no segregation defects in the wing, MadB1 bskflp147E clones can be used to study whether MadB1 affects segregation of cells at the A/P boundary. The majority of bskflp147E MadB1 clones of A origin in contact with the A/P boundary of the wing disc are misplaced into the P territory, causing a displacement of the A/P compartment boundary toward P. However, clones of P origin remain in the P compartment. brkXH MadB1/Mad12 clones generated along the A/P boundary of the wing imaginal disc, using the FLP/FRT technique, show no defects in segregation behaviour. As with wild-type clones, these mutant clones stay in the compartment (anterior or posterior) in which they have been generated.

Neural differentiation is blocked in smo2 ; MadB1 double mutant clones in the eye disc. Aberrant nuclear migration is seen in double mutant clones spanning the furrow.

At 18oC, 25oC and 29oC, Chc1/+, MadB1/+ double heterozygotes have normal wing patterns.

Homozygous MadB1 wgl-15 clones at the posterior margin of the eye disc autonomously fail to initiate photoreceptor development.

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

Complements: gktA12. Complements: gktG85.

Excision of the P{lacW} is accompanied by reversion of the Mad mutant phenotype.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (20)