FlyBase Allele Report: Dmel\AkhR[1]

General Information

Symbol

Dmel\AkhR¹

Species

D. melanogaster

Name

FlyBase ID

FBal0239233

Feature type

allele

Associated gene

Dmel\AkhR

Associated Insertion(s)

P{?EP}AkhR¹

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - molecular evidence

Mutagen

P-element activity

Nature of the Allele

Allele class

amorphic allele - molecular evidence

(Grönke et al., 2007)

Mutagen

P-element activity

(Grönke et al., 2007)

Progenitor genotype

P{EP}AkhR^G6244

(Grönke et al., 2007)

Associated Insertion(s)

P{?EP}AkhR¹

Cytology

Description

Imprecise excision of the progenitor insertion, resulting in a deletion of nucleotides -1448 to +3507 relative to the putative translation start site (genomic coordinates 2L:6711184-6716139 , release 4). This deletion removes the complete coding region. 289bp of residual P-element sequences remain.

(Grönke et al., 2007)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

delins

2L:6,711,184..6,716,139 [-]

Comment:

Deletion resulting from the imprecise excision of P{EP}AkhR^G6244. 289 bp of P-element sequence remain.

(Grönke et al., 2007)

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

(Baumbach et al., 2014, Grönke et al., 2007)

CEA with AkhR²

(Grönke et al., 2007)

CEA with bmm¹

(Grönke et al., 2007)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

exacerbates obesity

modeled by Lsd1¹

(Beller et al., 2010)

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal developmental rate

(Gáliková et al., 2015)

abnormal oxidative stress response | adult stage

(Gáliková et al., 2015)

abnormal starvation stress response | adult stage

(Gáliková et al., 2015)

abnormal starvation stress response | adult stage | recessive

(Yu et al., 2016)

abnormal stress response

(Beller et al., 2010)

decreased rate of movement | adult stage | recessive | nutrition conditional

(Yu et al., 2016)

Phenotype Manifest In

embryonic/larval midgut | third instar larval stage

(Palm et al., 2012)

lipid droplet

(Grönke et al., 2007)

lipid droplet (with AkhR²)

(Grönke et al., 2007)

Detailed Description

Statement

Reference

AkhR¹/AkhR¹ in adult females results in loss of the significant starvation-induced increase in locomotor activity seen in controls.

(Yu et al., 2016)

AkhR¹/AkhR¹ mutants do not display any abnormalities in hatchability, viability, female fecundity, body size (measured as length of thorax), wing area, adult spontaneous locomotion or climbing, flight performance, carbohydrate and lipid stores between L3 and immature adult stages, or carbohydrate stores in mature adults, as compared to controls.

AkhR¹/AkhR¹ mutants display a small, significant decrease in developmental time, In the first week of adulthood, AkhR¹/AkhR¹ mutants develop obesity (significantly increased glyceride to protein ratio), and adults show significantly decreased circulating sugars in the hemolymph. Adult AkhR¹/AkhR¹ mutants show significantly increased starvation resistance, impaired lipid (but not carbohydrate) mobilization during starvation, suppressed starvation-induced hyperactivity, increased survival in response to paraquat feeding, but also increased paraquat-induced food aversion, and decreased oxidative stress resistance when assayed by paraquat application directly to the nerve cord, as compared to controls.

(Gáliková et al., 2015)

Homozygous AkhR¹ mutants do not exhibit any day activity of sleep defects. Unlike in controls, treating AkhR¹ mutant flies with tolbutamide does not increase daytime activity.

(Metaxakis et al., 2014)

Triacylglycerol (TAG) accumulation in the guts of GRHR¹ 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 increase slightly.

(Palm et al., 2012)

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)

GRHR¹ and GRHR¹/GRHR² flies have an increased organismal fat content compared to control flies and accumulate lipid storage droplets in the fat body.

GRHR¹ flies show incomplete storage-fat mobilization in response to starvation.

GRHR¹ flies show resistance to starvation compared to control flies.

(Grönke et al., 2007)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Other

Statement

Reference

AkhR¹, Lsd1¹ has abnormal stress response phenotype

(Beller et al., 2010)

Phenotype Manifest In

NOT suppressed by

Statement

Reference

AkhR¹ has lipid droplet phenotype, non-suppressible by Scer\GAL4^fat/Akh^UAS.cLa

(Grönke et al., 2007)

Additional Comments

Genetic Interactions

Statement

Reference

AkhR¹ suppresses the increase in daytime activity seen in Df(3L)Ilp2-3, Ilp5¹ mutants. Night activity, night sleep duration and number of night sleep bouts are similar to controls. The increase in octopamine levels seen in Df(3L)Ilp2-3, Ilp5¹ mutant head extracts is also rescued by AkhR¹.

(Metaxakis et al., 2014)

Lipid levels are partially restored in GRHR¹ Sik3⁴⁸ double mutant flies.

(Wang et al., 2011)

Lsd-1¹ GRHR¹ double mutant flies are more obese than either single mutant. The double mutants show resistance to starvation compared to controls.

(Beller et al., 2010)

Expression of Akh^Scer\UAS.cLa under the control of Scer\GAL4^fat has no effect on the increased organismal fat content and accumulation of lipid storage droplets seen in GRHR¹ 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)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

AKHR¹

(Hughson et al., 2021, Choi et al., 2015, Chng et al., 2014, Wang et al., 2011, Beller et al., 2010, Grönke et al., 2007)

AkhR¹

(Meschi et al., 2024, Wat et al., 2021, Yoshinari et al., 2021, Hudry et al., 2019, Gáliková et al., 2015, Baumbach et al., 2014)

GRHR¹

akhr mutant

(Palm et al., 2012)

Name Synonyms

Secondary FlyBase IDs

References (16)

Report Sections

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