FlyBase Allele Report: Dmel\bgm[1]

General Information

Symbol

Dmel\bgm¹

Species

D. melanogaster

Name

FlyBase ID

FBal0098775

Feature type

allele

Associated gene

Dmel\bgm

Associated Insertion(s)

P{lacW}bgm¹

Carried in Construct

Key Links

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Min and Benzer, 1999)

Progenitor genotype

Associated Insertion(s)

P{lacW}bgm¹

Cytology

Description

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

(Min and Benzer, 1999)

Allele components

Component

Use(s)

Inserted element

P{lacW}

enhancer trap

Encoded product / tool

lacZ

reporter enzyme

Tagged with

Tag:NLS(P)

nuclear protein localization tag

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

Variant Molecular Consequences

Associated Sequence Data

DDBJ / EMBL / GenBank

DNA sequence

Protein sequence

UniProtKB/Swiss-Prot

UniProtKB/TrEMBL

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

model of adrenoleukodystrophy

CEA with hll¹

(Sivachenko et al., 2016)

CEA

(Gordon et al., 2018)

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

adult optic lobe

(Min and Benzer, 1999)

basement membrane | adult stage

(Sivachenko et al., 2016)

embryonic/larval gut | larval stage

(Sivachenko et al., 2016)

lamina

(Sivachenko et al., 2016, Min and Benzer, 1999)

lamina (with Df(2L)b87e25)

(Sivachenko et al., 2016)

lamina monopolar neuron

(Sivachenko et al., 2016)

ommatidium

(Sivachenko et al., 2016)

photoreceptor cell & axon

(Min and Benzer, 1999)

pigment cell

(Gordon et al., 2018)

retina

(Gordon et al., 2018, Sivachenko et al., 2016)

retina & cell body

(Min and Benzer, 1999)

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.

(Gordon et al., 2018)

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.

(Sivachenko et al., 2016)

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

(Thimgan et al., 2015)

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).

(Min and Benzer, 1999)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

bgm¹ has abnormal neuroanatomy | adult stage phenotype, enhanceable by hll¹/hll¹

(Sivachenko et al., 2016)

Enhancer of

Statement

Reference

bgm¹/bgm¹ is an enhancer of abnormal neuroanatomy | adult stage phenotype of hll¹

(Sivachenko et al., 2016)

NOT Enhancer of

Statement

Reference

bgm¹/bgm¹ is a non-enhancer of abnormal locomotor behavior | adult stage phenotype of hll¹

(Sivachenko et al., 2016)

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

(Sivachenko et al., 2016)

Other

Statement

Reference

bgm¹, hll¹ has viable phenotype

(Sivachenko et al., 2016)

Phenotype Manifest In

Enhanced by

Statement

Reference

bgm¹ has lamina phenotype, enhanceable by hll¹/hll¹

(Sivachenko et al., 2016)

NOT Enhanced by

Statement

Reference

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

(Sivachenko et al., 2016)

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

(Sivachenko et al., 2016)

Enhancer of

Statement

Reference

bgm¹/bgm¹ is an enhancer of lamina phenotype of hll¹

(Sivachenko et al., 2016)

bgm¹/bgm¹ is an enhancer of retina phenotype of hll¹

(Sivachenko et al., 2016)

bgm¹/bgm¹ is an enhancer of basement membrane | adult stage phenotype of hll¹

(Sivachenko et al., 2016)

Other

Statement

Reference

bgm¹, hll¹ has ommatidium phenotype

(Sivachenko et al., 2016)

bgm¹, hll¹ has secondary pigment cell phenotype

(Sivachenko et al., 2016)

bgm¹, hll¹ has lamina monopolar neuron phenotype

(Sivachenko et al., 2016)

bgm¹, hll¹ has embryonic/larval gut | larval stage phenotype

(Sivachenko et al., 2016)

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.

(Sivachenko et al., 2016)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

bgm¹ is rescued by bgm^UAS.Tag:FLAG/Scer\GAL4^αTub84B.PL

(Gordon et al., 2018)

bgm¹ is rescued by bgm^UAS.Tag:FLAG/Scer\GAL4^sim.P3.7

(Gordon et al., 2018)

Not rescued by

bgm¹ is not rescued by Scer\GAL4^repo/bgm^UAS.Tag:FLAG

(Gordon et al., 2018)

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

28120

w^*; P{lacW}bgm¹

Notes on Origin

Discoverer

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.

(Min and Benzer, 1999)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

bgm¹

(Gordon et al., 2018, Sivachenko et al., 2016, Thimgan et al., 2015)

Name Synonyms

Secondary FlyBase IDs

References (4)

Report Sections

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