FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
Allele: Dmel\Met1
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General Information
Symbol
Dmel\Met1
Species
D. melanogaster
Name
FlyBase ID
FBal0014802
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
Met
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Cytology
Description

Amino acid replacement: G166D.

Mutations Mapped to the Genome
Curation Data
Type
Location
Additional Notes
References
Nucleotide change:

G11617364A

Amino acid change:

G166D | Met-PA; G166D | Met-PB

Reported amino acid change:

G166D

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

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

Homozygotes show increased resistance to methoprene compared to controls.

18% of mutant flies have a small number of defective ommatidia in the posterior quarter of the eye.

Homozygotes fed 100μl methoprene have almost normal optic lobes, except for a very small defect in the right outer chiasm, in contrast to wild-type flies, which show widespread degeneration of the optic lobes after feeding with 100μl methoprene. In addition, homozygotes occasionally show very mild subesophageal ganglion-thoracic ganglion (SEG-TG) fusion defects when fed 100μl methoprene, in contrast to wild-type flies, which show severe SEG-TG fusion defects when fed 100μl methoprene. Homozygotes have slightly reduced numbers of muscle fibres in the retractor muscles of the rostrum of the proboscis when fed 100μl methoprene.

Homozygous, heterozygous, hemizygous and Rst(1)JHD29/Rst(1)JH1 larvae show increased resistance to Methoprene compared to wild-type. Homozygous, hemizygous and Rst(1)JHD29/Rst(1)JH1 adults derived from larvae treated with Methoprene have normal bristle patterns on sternites 6 and 7, in contrast to wild-type adults derived from larvae treated with Methoprene, which have disrupted bristle patterns on these sternites.

Flies carrying Rst(1)JH1 have a competitive disadvantage compared to wild-type flies. Pupal survival is reduced compared to wild-type.

Rst(1)JH1 mutants are 10 times more resistant than wild-type to S31183 (2-1-methyl-2-(4-phenoxyphenoxy)-ethoxy-pyridine), a juvenile hormone mimic, in a white puparial assay and about 20 times more resistant than wild-type to S31183 in a larval feeding assay.

Strong allele. Only minor differences in penetration, excretion, sequestration and metabolism of juvenile hormone III are detected in Rst(1)JH1 flies compared to Rst(1)JH+ flies. Rst(1)JH1 flies have an approximately 10-fold lower binding affinity for juvenile hormone III than Rst(1)JH+ flies.

Juvenile hormone III binding affinity and total protein accumulation in the male accessory glands is reduced.

Slightly stronger than Rst(1)JH2. Homozygotes are nearly two orders of magnitude (100x) more resistant to methoprene and juvenile hormone III than wild-type. The resistance of heterozygotes is intermediate between the homozygote and wild-type. Also resistant to methoprene induced morphogenetic abnormalities and tumours.

Semidominant mutation conferring 50-100 fold increase in resistance to juvenile hormone III or its analogue methoprene over that of wild type. Also resistant to methoprene-induced tumors and abnormalities in adult cuticle; action of Rst(1)JH autonomous in gynandromorphs. Wilson speculates that gene may affect juvenile-hormone receptor.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Phenotype Manifest In
NOT Enhancer of
Statement
Reference
Suppressor of
NOT Suppressor of
Statement
Reference
Other
Additional Comments
Genetic Interactions
Statement
Reference
Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Comments
Images (0)
Mutant
Wild-type
Stocks (2)
Notes on Origin
Discoverer
Comments
Comments

Analysis of gynandromorphs shows that Rst(1)JH1 acts autonomously.

The fitness component(s) responsible for the competitive disadvantage of flies carrying mutant alleles of Rst(1)JH have been analysed in Rst(1)JH1, Rst(1)JH2, Rst(1)JH3, Rst(1)JHD29 and Rst(1)JHN6 flies. Small but significant differences were found between the pooled Rst(1)JH alleles and wild-type for pupal developmental time, pupal mortality, and early adult fecundity. These differences results in a large competitive disadvantage.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (4)
References (15)