FlyBase Allele Report: Dmel\Act88F[6]

General Information

Symbol

Dmel\Act88F⁶

Species

D. melanogaster

Name

FlyBase ID

FBal0000272

Feature type

allele

Associated gene

Dmel\Act88F

Associated Insertion(s)

Carried in Construct

Also Known As

Act88F^KM88, KM88

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - genetic evidence

hypomorphic allele - genetic evidence

Mutagen

Nature of the Allele

Allele class

amorphic allele - genetic evidence

(Cripps et al., 1994, Nelson and Szauter, 1992, Beall et al., 1989)

hypomorphic allele - genetic evidence

(Fyrberg et al., 1988)

Mutagen

Progenitor genotype

Cytology

Description

Amino acid replacement: W79term.

(Fyrberg et al., 1988)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

3R:15,440,854..15,440,854 [+]

Nucleotide change:

G15440854A

Amino acid change:

W80term | Act88F-PA

Reported amino acid change:

W79term

Comment:

G to A nucleotide change at the second or third position of the wild type Trp codon leads to a nonsense mutation (exact site of mutation unspecified). The mutation was annotated at the second base of the codon.

(Fyrberg et al., 1988)

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 nemaline myopathy

CEA

(Gautam et al., 2015)

model of congenital structural myopathy

CEA with Act88F^R372H

(Haigh et al., 2010)

model of myopathy

CEA with cher^EPSΔ5

(González-Morales et al., 2017)

CEA with cher¹

(González-Morales et al., 2017)

CEA with cher^CPTI001403

(González-Morales et al., 2017)

DOES NOT model myopathy

CEA with cher^sko

(González-Morales et al., 2017)

model of hypertrophic cardiomyopathy 11

CEA with Act88F^A331P

(Doran et al., 2025)

CEA

(Doran et al., 2025)

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

abnormal flight, with Act88F^+tMa

(Viswanathan et al., 2017)

abnormal flight, with Act88F^A296S

(Viswanathan et al., 2017)

abnormal flight, with Act88F^I136M

(Sevdali et al., 2013)

abnormal flight | dominant

(Reedy et al., 2000)

abnormal locomotor behavior | recessive

(Nongthomba et al., 2001)

decreased rate of flight behavior, with Act88F^A331P

(Doran et al., 2025)

decreased size | adult stage, with Act88F^A331P

(Doran et al., 2025)

female semi-fertile | recessive

(Nongthomba et al., 2001)

flightless

(Doran et al., 2025, Viswanathan et al., 2020)

flightless, with Act88F^+tMa

(Viswanathan et al., 2017)

flightless, with Act88F^A331P

(Doran et al., 2025)

flightless, with Act88F^D154N

(Sevdali et al., 2013)

flightless, with Act88F^D292V

(Sevdali et al., 2013)

flightless, with Act88F^G15R

(Sevdali et al., 2013)

flightless, with Act88F^V163L

(Sevdali et al., 2013)

flightless, with Act88F^V163M

(Sevdali et al., 2013)

flightless | dominant

flightless | recessive

(Brault et al., 1999)

viable

(Brault et al., 1999)

Phenotype Manifest In

adult somatic muscle cell

(Gautam et al., 2015)

dorsal longitudinal indirect flight muscle, with Act88F^A331P

(Doran et al., 2025)

dorsal longitudinal indirect flight muscle cell

(Nongthomba et al., 2004)

dorsal longitudinal indirect flight muscle cell | adult stage, with Act88F^A296S

(Viswanathan et al., 2017)

filamentous actin | adult stage

(Doran et al., 2025)

indirect flight muscle & muscle tendon junction

(Brault et al., 1999)

indirect flight muscle & striated muscle thick filament

(Brault et al., 1999)

indirect flight muscle & striated muscle thin filament

(Reedy et al., 2000, Brault et al., 1999)

indirect flight muscle cell

(Liao et al., 2020, Molnár et al., 2014)

indirect flight muscle cell, with Act88F^D154N

(Sevdali et al., 2013)

indirect flight muscle cell, with Act88F^D292V

(Sevdali et al., 2013)

indirect flight muscle cell, with Act88F^G15R

(Sevdali et al., 2013)

indirect flight muscle cell, with Act88F^I136M

(Sevdali et al., 2013)

indirect flight muscle cell, with Act88F^M306L

(Viswanathan et al., 2020)

indirect flight muscle cell, with Act88F^V163L

(Sevdali et al., 2013)

indirect flight muscle cell, with Act88F^V163M

(Sevdali et al., 2013)

indirect flight muscle cell | adult stage

(González-Morales et al., 2017)

myofibril

(Liao et al., 2020)

myofibril, with Act88F^D154N

(Sevdali et al., 2013)

myofibril, with Act88F^D292V

(Sevdali et al., 2013)

myofibril, with Act88F^G15R

(Sevdali et al., 2013)

myofibril, with Act88F^I136M

(Sevdali et al., 2013)

myofibril, with Act88F^V163L

(Sevdali et al., 2013)

myofibril, with Act88F^V163M

(Sevdali et al., 2013)

myofibril | adult stage

(González-Morales et al., 2017)

myofibril | adult stage, with Act88F^A331P

(Doran et al., 2025)

sarcomere

(Liao et al., 2020)

sarcomere | adult stage, with Act88F^A331P

(Doran et al., 2025)

striated muscle thin filament

(Molnár et al., 2014)

tendon cell

(Brault et al., 1999)

wing

(Nongthomba et al., 2001)

Z disc, with Act88F^D154N

(Sevdali et al., 2013)

Z disc, with Act88F^D292V

(Sevdali et al., 2013)

Z disc, with Act88F^G15R

(Sevdali et al., 2013)

Z disc, with Act88F^I136M

(Sevdali et al., 2013)

Z disc, with Act88F^V163L

(Sevdali et al., 2013)

Z disc, with Act88F^V163M

(Sevdali et al., 2013)

Detailed Description

Statement

Reference

Homozygous expression of Act88F^M306L in Act88F⁶ background leads to morphological defects in adult indirect muscles when compared to controls.

(Viswanathan et al., 2020)

In Act88F⁶ heterozygotes, the indirect flight muscle sarcomeres appear relatively normal except for the occasional splitting of myofibrils, as compared to controls.

(González-Morales et al., 2017)

Act88F⁶ heterozygotes bearing one copy of Act88F^+tMa or Act88F^A295S do not present significant changes in average body weight but exhibit mild and more severe significant defects in flight performance, as compared to controls: a significant decrease in flight index assessed by standard flight assays; significant decreases in overall and angular velocity and significant decreases in centripetal acceleration, assessed by digital inline holography. Act88F⁶ heterozygotes bearing one copy of Act88F^A295S, but not Act88F^+tMa, also exhibit a significant decrease in overall acceleration. Act88F⁶ homozygotes bearing tow copy of either Act88F^+tMa or Act88F^A295S are flightless.

(Viswanathan et al., 2017)

Raman spectroscopy reveals that, as muscle degeneration progresses with age, Act88F⁶ mutant muscles show a significant increase in the levels of glycogen and carotenoids compared with wild-type controls.

(Gautam et al., 2015)

Heterozygotes show mild defects in the indirect flight muscles: myofibrils are thinner than normal some Z-discs are not entirely straight. The precisely repeating organisation of the sarcomeres is retained.

(Molnár et al., 2014)

Flies carrying one copy of Act88F^I136M in a Act88F⁶/+ background show reduced flight ability.

Flies carrying one copy of either Act88F^G15R, Act88F^D154N, Act88F^V163L, Act88F^V163M or Act88F^D292V in a Act88F⁶/+ background are completely flightless.

Flies carrying one copy of Act88F^D292V in a Act88F⁶/+ background show intermediate defects in myofibril organisation in the indirect flight muscles. Z-discs are less regular than normal. The defects are milder in flies carrying two copies of Act88F^D292V in a homozygous Act88F⁶ background.

Flies carrying one copy of Act88F^I136M in a Act88F⁶/+ background show intermediate defects in myofibril organisation in the indirect flight muscles. The defects are stronger in flies carrying two copies of Act88F^I136M in a homozygous Act88F⁶ background.

Flies carrying one copy of Act88F^G15R in a Act88F⁶/+ background show intermediate defects in myofibril organisation in the indirect flight muscles. Z-discs are less regular than normal. The defects are stronger in flies carrying two copies of Act88F^G15R in a homozygous Act88F⁶ background.

Flies carrying one copy of Act88F^D154N in a Act88F⁶/+ background show major defects in Z-disc organisation in the indirect flight muscles. Recognisable ordered myofibrils are not formed in the indirect flight muscles of flies carrying two copies of Act88F^D154N in a homozygous Act88F⁶ background, although disordered actin filaments are present.

Flies carrying one copy of Act88F^V163M in a Act88F⁶/+ background show major defects in Z-disc organisation in the indirect flight muscles. Recognisable ordered myofibrils are not formed in the indirect flight muscles of flies carrying two copies of Act88F^V163M in a homozygous Act88F⁶ background, although disordered actin filaments are present.

Flies carrying one copy of Act88F^V163L in a Act88F⁶/+ background show major defects in Z-disc organisation in the indirect flight muscles.

Closely packed Z-disc stacks or "zebra bodies" are seen in the indirect flight muscles of flies carrying one copy of either Act88F^G15R, Act88F^I136M, Act88F^D154N or Act88F^D292V in a Act88F⁶/+ background.

Closely packed Z-disc stacks or "zebra bodies" are seen in the indirect flight muscles of flies carrying one copy of Act88F^V163M in a Act88F⁶/+ background. Areas in which Z-discs appear to be splitting apart are also seen.

Areas in which Z-discs appear to be splitting apart are seen in the indirect flight muscles of flies carrying one copy of Act88F^V163L in a Act88F⁶/+ background.

Ring-like Z-disc structures or aggregates and F-actin containing intranuclear rods are seen in the indirect flight muscles of flies carrying one copy of either Act88F^V163M, Act88F^D154N or Act88F^V163L in a Act88F⁶/+ background.

(Sevdali et al., 2013)

The jump muscle output of 4 day old Act88F⁶ flies (measured using displacement of an ergometer) is increased compared to control flies.

(Elliott et al., 2007)

The dorsal longitudinal muscles of Act88F⁶ mutant flies develop a fibre morphology that appears "wiggly" with the fibres bulging out in some areas and constricted in many areas. Occasionally these fibres seem to be partly split and appear not to fit within the thorax.

(Nongthomba et al., 2004)

Homozygotes show poor walking ability. Females produce significantly fewer eggs than wild type, and progeny consequently complete a major part of their development in utero. Adults show a slight dishing of the wing blade.

(Nongthomba et al., 2001)

Mutants completely lack thin filaments in the indirect flight muscle, but do have a large number of thick filaments that form bundles. Heterozygotes have a flight impairment (flight index is 0.1 +/- 0.3 compared to 5.6 +/- 1.1 for wild-type).

(Reedy et al., 2000)

The modified terminal Z-discs (MT-Zs) of the myotendon junction are absent in indirect flight muscles. The dense junctions normally seen between the membranes of the muscle and tendon cells are also missing. The membrane surrounding the muscle cells balloons and blebs, creating vacuoles between the muscle and tendon cells. The morphology of the tendon cells is almost normal.

(Brault et al., 1999)

Homozygotes are flightless. The thick filaments of the indirect flight muscle appear to be more or less randomly distributed and thin filaments are not evident.

(Brault et al., 1999)

Comparison of the myofibrillar proteins from the demembranated indirect flight muscles of heterozygotes and homozygotes demonstrate a pleiotropic effect upon the accumulation of actin-associated myofibrillar proteins. Actin, troponin-H, troponin-I, troponin-T and tropomyosin are missing in the homozygote.

(Cripps et al., 1994)

No thin filaments or Z discs are present in Act88F⁶ homozygotes. In Mhc⁷; Act88F⁶ double homozygotes mitochondria and nuclei are the only recognizable organelles, thick and thin filaments are needed for sarcomere order and periodicity. Flight muscle defects are due to an imbalance in actin and myosin accumulation. Heterozygotes have longer sarcomeres than wild type: filament stoichiometry influences sarcomere length determination.

(Beall et al., 1989)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Act88F⁶, Act88F^D292V has flightless phenotype, suppressible by up¹⁰¹

(Sevdali et al., 2013)

Act88F⁶, Act88F^D292V has flightless phenotype, suppressible by wupA^hdp-2

(Sevdali et al., 2013)

Act88F⁶ has abnormal flight | dominant phenotype, suppressible by Mhc[+]/Mhc⁷

(Reedy et al., 2000)

Act88F⁶ has abnormal flight | dominant phenotype, suppressible by fln⁰/fln[+]

(Reedy et al., 2000)

Suppressor of

Statement

Reference

Act88F⁶/Act88F[+] is a suppressor of abnormal flight | dominant phenotype of Mhc⁷

(Reedy et al., 2000)

Phenotype Manifest In

Enhanced by

Statement

Reference

Act88F⁶ has myofibril phenotype, enhanceable by Zasp52^MI02988

(Liao et al., 2020)

Act88F⁶ has sarcomere phenotype, enhanceable by Zasp52^MI02988

(Liao et al., 2020)

Act88F⁶ has indirect flight muscle cell phenotype, enhanceable by Zasp52^MI02988

(Liao et al., 2020)

Act88F⁶ has indirect flight muscle cell phenotype, enhanceable by DAAM^Ex1/DAAM^Ex1

(Molnár et al., 2014)

Suppressed by

Statement

Reference

Act88F⁶ has dorsal longitudinal indirect flight muscle cell phenotype, suppressible by Mhc⁷

(Nongthomba et al., 2004)

Act88F⁶ has indirect flight muscle & muscle tendon junction phenotype, suppressible by Hsap\ACTB^{Act88F.StuI.EcoRI}

(Brault et al., 1999)

Act88F⁶ has tendon cell phenotype, suppressible by Hsap\ACTB^{Act88F.StuI.EcoRI}

(Brault et al., 1999)

Enhancer of

Statement

Reference

Act88F⁶/Act88F[+] is an enhancer of indirect flight muscle cell phenotype of DAAM^Ex1

(Molnár et al., 2014)

Other

Statement

Reference

Act88F⁶, cher^EPSΔ5 has sarcomere | adult stage phenotype

(González-Morales et al., 2017)

Act88F⁶, cher^EPSΔ5 has indirect flight muscle cell | adult stage phenotype

(González-Morales et al., 2017)

Act88F⁶, cher¹ has sarcomere | adult stage phenotype

(González-Morales et al., 2017)

Act88F⁶, cher¹ has indirect flight muscle cell | adult stage phenotype

(González-Morales et al., 2017)

Act88F⁶, cher^CPTI001403 has sarcomere | adult stage phenotype

(González-Morales et al., 2017)

Act88F⁶, cher^CPTI001403 has indirect flight muscle cell | adult stage phenotype

(González-Morales et al., 2017)

Additional Comments

Genetic Interactions

Statement

Reference

Act88F⁶, cher^EPSΔ5 double heterozygotes, Act88F⁶, cher¹ double heterozygotes or Act88F⁶, cher^CPTI001403 double heterozygotes, but not Act88F⁶, cher^sko double heterozygotes, frequently present myofibrils that are too frayed to distinguish individual sarcomeres, as compared to the corresponding single heterozygous controls.

(González-Morales et al., 2017)

The mild indirect muscle phenotype seen in DAAM^Ex1 mutants is strongly enhanced by Act88F⁶/+. The double mutants have a network of very thin myofibrils which often appear branched and the regular Z-disc and sarcomere organisation is completely abolished.

(Molnár et al., 2014)

In double homozygote Act88F⁶/Mhc⁷ mutants, dorsal longitudinal muscle fibres appear no different from in wild-type flies.

(Nongthomba et al., 2004)

One copy of fln⁰ partially restores the flight ability of Act88F⁶ heterozygotes (flight index of double heterozygotes is 3.4 +/- 1.7). Act88F⁶ Mhc⁷ double heterozygotes have a flight index of 3.3 +/- 1.2.

(Reedy et al., 2000)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Act88F⁶ is rescued by Act88F^StuI.EcoRI

(Brault et al., 1999)

Act88F⁶ is rescued by Act88F^-3'UTR

(Brault et al., 1999)

Act88F⁶ is rescued by Act88F^cBa

(Brault et al., 1999)

Partially rescued by

Act88F⁶ is partially rescued by Act88F^N.Tag:VSV-G

(Brault et al., 1999)

Act88F⁶ is partially rescued by Act88F^{N.Tag:polyHis}

(Brault et al., 1999)

Act88F⁶ is partially rescued by Act88F^E334K

(Drummond et al., 1991)

Act88F⁶ is partially rescued by Act88F^G366D

(Drummond et al., 1991)

Act88F⁶ is partially rescued by Act88F^R372H

(Drummond et al., 1991)

Act88F⁶ is partially rescued by Act88F^G368E

(Drummond et al., 1991)

Act88F⁶ is partially rescued by Act88F^E316K

(Drummond et al., 1991)

Act88F⁶ is partially rescued by Act88F^V339I

(Drummond et al., 1991)

Act88F⁶ is partially rescued by Act88F^E364K

(Drummond et al., 1991)

Not rescued by

FBal0335752:, Act88F⁶ is not rescued by Act88F^+tMa/Act88F^+tMa

(Viswanathan et al., 2020)

FBal0362574:, Act88F⁶ is not rescued by Act88F^M306L/Act88F^M306L

(Viswanathan et al., 2020)

Act88F⁶ is not rescued by Act88F^-5'UTR

(Brault et al., 1999)

Act88F⁶ is not rescued by Act88F^C.Tag:VSV-G

(Brault et al., 1999)

Act88F⁶ is not rescued by Act88F^{C.Tag:polyHis}

(Brault et al., 1999)

Comments

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Comments

Actin III entirely absent from indirect flight muscle in homozygotes; levels of actin II also reduced.

(Hiromi and Hotta, 1985)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (6)

Reported As

Symbol Synonym

Act88F-null

(Doran et al., 2025)

Act88F⁶

(Elliott et al., 2007)

At88F^KM88

(Anson et al., 1995)

KM88

(Viswanathan et al., 2020, Viswanathan et al., 2017, Haigh et al., 2010, Reedy et al., 2000, Schmitz et al., 2000, Brault et al., 1999, Razzaq et al., 1999, Schoenenberger et al., 1995, Vigoreaux, 1994, Maughan et al., 1991, Fyrberg and Beall, 1990)

Name Synonyms

actin88FKM88

(Gautam et al., 2015)

Secondary FlyBase IDs

References (42)

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