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General Information
Symbol
Dmel\bgm1
Species
D. melanogaster
Name
FlyBase ID
FBal0098775
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Allele class
Nature of the Allele
Allele class
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

A P{lacZ} element is inserted in the first intron which splits the 5'UTR of bgm.

Insertion components
P{lacW}bgm1
Product class / Tool use(s)
Encoded product / tool
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 ( 1 )
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

bgm1 flies present holes in the retina and disrupted pigment cells between ommatidia. This phenotype is reduced in flies raised in constant dark and exacerbated under constant light conditions.

bgm1/bgm1 and bgm1/Df(2L)b87e25 mutant flies exhibit degeneration of the lamina, as assayed by holes in the optic ganglion at 18 days old, but these holes are not seen in newly eclosed flies; these mutants do not exhibit rough eye phenotypes. bgm1/bgm1 mutants show retinal holes, thinning and irregularity of the fenestrated membrane between the retina and lamina, disarray of the ommatidial structure not visible in newly eclosed flies but apparent at day 20, disorganization of photoreceptor axons in the lamina, cell death of monopolar neurons, abnormal inclusions in the lamina, decreased locomotor activity not evident in newly eclosed flies but apparent by 7 days, evidence of increased lipid accumulation in the larval gut as compared to wild type, but no significant decrease in lifespan.

bgm1 mutants display a significantly larger sleep rebound following 12 hrs of sleep deprivation, compared to controls.

Brain degeneration mutant In young homozygous mutant flies, the optic lobes appear normal but, with age regionally specific degeneration develops. This is particularly marked in the first optic ganglion, the lamina, in which photoreceptor axons enter to synapse with second-order neurons. The lamina has a bubbly appearance. There is also degeneration of the cell bodies in the retina. Electron micrographs show inflation of various structures, which is most evident in the expansion in the diameter of the photoreceptor axons. Mutant flies perform poorly in countercurrent phototaxis tests (flies respond in 10% of all trials).

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
Enhancer of
Statement
Reference
NOT Enhancer of
Statement
Reference

bgm1/bgm1 is a non-enhancer of short lived phenotype of hll1

Other
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference

bgm1 has lamina phenotype, enhanceable by hll1/hll1

NOT Enhanced by
Statement
Reference

bgm1 has retina phenotype, non-enhanceable by hll1/hll1

bgm1 has basement membrane | adult stage phenotype, non-enhanceable by hll1/hll1

Enhancer of
Statement
Reference

bgm1/bgm1 is an enhancer of lamina phenotype of hll1

bgm1/bgm1 is an enhancer of retina phenotype of hll1

Other
Additional Comments
Genetic Interactions
Statement
Reference

bgm1/bgm1, hll1/hll1 double mutants exhibit more severe degeneration of the lamina, as assayed by holes in the optic ganglion at 18 days old, than either single mutant, and degeneration of the retina and fenestrated membrane structure was more severe in double mutants than hll1/hll1 single mutants, but not statistically different from bgm1/bgm1 single mutants. bgm1/bgm1, hll1/hll1 double mutants show retinal holes, thinning and irregularity of the fenestrated membrane between the retina and lamina, disarray of the ommatidial structure not visible in newly eclosed flies but apparent at day 20, and loss of monopolar neurons (often associated with abnormal extracellular precipitates), loss of secondary pigment cells, decreased locomotor activity to a similar degree as single mutants, a small decrease in lifespan, evidence of increased lipid accumulation in the larval gut, but not in the adult eye, as compared to wild type. These mutants do not exhibit a rough eye phenotype.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer
Comments
Comments

When treated with Glyceryl trioleate oil (GTO, a component of "Lorenzo's Oil"), from larvae until adulthood, both the physiological defects and the phototaxis defects were at least partially rescued. If fed from young adulthood, the beneficiary effects were much less great.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (1)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (4)