FlyBase Allele Report: Dmel\bmm[1]

General Information

Symbol

Dmel\bmm¹

Species

D. melanogaster

Name

FlyBase ID

FBal0195572

Feature type

allele

Associated gene

Dmel\bmm

Associated Insertion(s)

P{3'EP}bmm¹

Carried in Construct

Key Links

Allele class

loss of function allele

Mutagen

P-element activity

Nature of the Allele

Allele class

loss of function allele

(Gronke et al., 2005)

Mutagen

P-element activity

(Gronke et al., 2005)

Progenitor genotype

bmm^EP3174

(Gronke et al., 2005)

Associated Insertion(s)

P{3'EP}bmm¹

Cytology

Description

bmm¹ was generated by mobilization of P{EP}bmm^EP3174 and is a deletion mutant lacking DNA sequences from position 5006-9479 relative to the putative start ATG, causing lack of bmm amino acids 52-507. bmm¹ contains residual 3' P element sequences.

(Gronke et al., 2005)

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 obesity

CEA

(Kim et al., 2020, Grönke et al., 2007)

CEA with AkhR¹

(Grönke et al., 2007)

model of acquired metabolic disease

CEA

(Mirzoyan et al., 2023)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

exacerbates obesity

modeled by Lsd-1¹

(Beller et al., 2010)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

Detailed Description

Statement

Reference

bmm¹ testes exhibit increased number of lipid droplets in somatic cells.

bmm¹ males and females exhibit increased starvation resistance in both males and females.

(Wat et al., 2020)

triacylglycerol (TAG) accumulation in the guts of bmm¹ mutant larvae is biased towards medium-chain species. Medium-chain diacylglycerol (DAG) levels are not reduced in the hemolymph but levels of medium-chain DAG in the gut are increased slightly.

(Palm et al., 2012)

bmm¹ mutants have no ectopic lipid storage in salivary glands.

(Tian et al., 2011)

Mutant flies have an increased fat content and show increased starvation resistance compared to controls. The mutant flies show incomplete storage fat mobilisation under starvation conditions.

(Beller et al., 2010)

Mutant flies have an increased organismal fat content compared to control flies.

bmm¹ flies show incomplete storage-fat mobilization in response to starvation.

bmm¹ flies show resistance to starvation compared to control flies.

(Grönke et al., 2007)

Embryos maternally and zygotically mutant for bmm¹ display pleiotropic degeneration phenotypes and only approximately 1.7% hatch.

Zygotically mutant bmm¹ flies develop normally but show progressive obesity accumulating 17% (as immature adults, less than 1 day old) to 101% (as mature adults, 6 days old) more storage fat (measured as triacylglycerol content) compared to control (bmm^rev) flies.

Immature adult bmm¹ mutant fat body cells show variously sized storage droplets.

Mature bmm¹ mutant adults show no difference in carbohydrate storage (measured as glycogen content) compared to controls.

The median lifespan of (fed) bmm¹ flies is reduced by 10% compared to (fed) control (bmm^rev) flies.

Acute storage fat (triacylglycerol) mobilization in bmm¹ flies is impaired: during starvation, bmm¹ mutants consume 73% of their prestarvation fat content whereas control (bmm^rev) flies deplete their storage fat. Accordingly, starved bmm¹ mutant flies outlive starved controls by 56% on the expense of their prestarvation fat storage. bmm¹ mutants fuel their extended survival during starvation by metabolizing 65% more triacylglycerol than control (bmm^rev) flies.

Approximately 39.3% of bmm^rev/bmm¹ embryos, in which the revertant bmm^rev allele is paternally supplied, hatch.

(Gronke et al., 2005)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Other

Statement

Reference

Lsd-1¹, bmm¹ has abnormal stress response phenotype

(Beller et al., 2010)

Phenotype Manifest In

Suppressed by

Statement

Reference

bmm¹ has phenotype, suppressible by Lsd-2⁵¹

(Gronke et al., 2005)

Enhancer of

Statement

Reference

bmm¹ is an enhancer of embryonic/larval fat body | larval stage phenotype of Lsd-1³⁸

(Bi et al., 2012)

bmm¹ is an enhancer of lipid droplet phenotype of Lsd-1³⁸

(Bi et al., 2012)

bmm¹ is an enhancer of embryonic/larval fat body | larval stage phenotype of Hsl^b24

(Bi et al., 2012)

bmm¹ is an enhancer of lipid droplet phenotype of Hsl^b24

(Bi et al., 2012)

Suppressor of

Statement

Reference

bmm¹ is a suppressor of phenotype of Lsd-2⁵¹

(Gronke et al., 2005)

Other

Statement

Reference

Pxt^unspecified, bmm¹ has egg chamber phenotype

(Giedt et al., 2023)

Pxt^unspecified, bmm¹ has actin filament bundle | oogenesis phenotype

(Giedt et al., 2023)

Pxt^unspecified, bmm¹ has cortical actin cytoskeleton | oogenesis phenotype

(Giedt et al., 2023)

Additional Comments

Genetic Interactions

Statement

Reference

The increase in size of the lipid droplets in the fat body of Hsl^b24 homozygous larvae is enhanced if they are also mutant for bmm¹.

The large lipid droplet phenotype seen in Lsd-1³⁸ larvae is enhanced by bmm¹.

(Bi et al., 2012)

Lipid levels are completely restored in bmm¹ Sik3⁴⁸ double mutant flies.

(Wang et al., 2011)

Lsd-1¹ bmm¹ double mutant flies are more obese than either single mutant and the double mutants fail to mobilise their fat storage under starvation conditions are hypersensitive to starvation.

(Beller et al., 2010)

Expression of Akh^Scer\UAS.cLa under the control of Scer\GAL4^fat reduces the increased organismal fat content seen in bmm¹ mutant flies.

bmm¹ GRHR¹ double mutant flies show an additive phenotype with respect to excess accumulation of body fat and lipid droplets. These double mutants die rapidly after food deprivation, and cannot mobilise even part of their excessive fat stores in response to starvation.

(Grönke et al., 2007)

bmm¹, Lsd-2⁵¹ double mutants have wild type fat storage levels (as measured by triacylglycerol content), indicating that loss of Lsd-2 compensates for lack of bmm and vice versa.

(Gronke et al., 2005)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

bmm¹ is rescued by Scer\GAL4^Act5C.PI/bmm^UAS.cGa

(Gronke et al., 2005)

bmm¹ is rescued by bmm^UAS.EGFP/Scer\GAL4^Act5C.PI

(Gronke et al., 2005)

Partially rescued by

bmm¹ is partially rescued by Scer\GAL4^Act5C.PI/bmm^UAS.cGa

(Gronke et al., 2005)

Comments

Expression of bmm^Scer\UAS.cGa under the control of Scer\GAL4^Act5C.PI almost completely rescues the lethality of embryos maternally and zygotically mutant for bmm¹.

Expression of bmm^Scer\UAS.cGa under the control of Scer\GAL4^Act5C.PI reverts the obese phenotype of bmm¹ mutant flies.

Expression of bmm^{Scer\UAS.T:Avic\GFP-EGFP} under the control of Scer\GAL4^Act5C.PI reverts the obese phenotype of bmm¹ mutant flies.

(Gronke et al., 2005)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

98123

w^*; bmm¹/TM3, Sb⁺

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

Bmm¹

(Meschi et al., 2024)

bmm mutant

(Palm et al., 2012)

bmm¹

(Giedt et al., 2023, Mirzoyan et al., 2023, Girard et al., 2021, Heier et al., 2021, Wat et al., 2021, Kim et al., 2020, Wat et al., 2020, Hehlert et al., 2019, May et al., 2019, Gáliková et al., 2017, Diop et al., 2015, Bi et al., 2012, Wang et al., 2012, Tian et al., 2011, Wang et al., 2011, Beller et al., 2010, Sieber and Thummel, 2009, Grönke et al., 2007, Gronke et al., 2005)

Name Synonyms

Secondary FlyBase IDs

References (22)

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