FlyBase Allele Report: Dmel\sws[1]

General Information

Symbol

Dmel\sws¹

Species

D. melanogaster

Name

FlyBase ID

FBal0016670

Feature type

allele

Associated gene

Dmel\sws

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

Mutagen

ethyl methanesulfonate

Progenitor genotype

Cytology

Description

The sws¹ mutation produces a truncated polypeptide that terminates at residue 375, thus lacking the esterase domain.

(Muhlig-Versen et al., 2005)

Nucleotide substitution: C1616A.

(Kretzschmar et al., 1997)

Amino acid replacement: S375term.

(Kretzschmar et al., 1997)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

X:7,963,853..7,963,853 [-]

Nucleotide change:

C7963853A

Reported nucleotide change:

C1616A

Amino acid change:

S375term | sws-PA; S375term | sws-PC

Reported amino acid change:

S375term

(Kretzschmar et al., 1997)

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 cerebellar ataxia

CEA

(Topaloglu et al., 2014)

model of hereditary spastic paraplegia

CEA

(Dutta et al., 2016)

model of blindness

CEA

(Kmoch et al., 2015)

model of neurodegenerative disease

CEA

(Melentev et al., 2021, Sunderhaus et al., 2019, Krishnan et al., 2012)

model of Oliver-McFarlane syndrome

CEA with Hsap\PNPLA6^L524P.UAS

(Sunderhaus et al., 2019)

CEA with Hsap\PNPLA6^R1099Q.UAS

(Sunderhaus et al., 2019)

model of Boucher-Neuhauser syndrome

CEA with Hsap\PNPLA6^G578W.UAS

(Sunderhaus et al., 2019)

model of Gordon Holmes syndrome

CEA with Hsap\PNPLA6^T629R.UAS

(Sunderhaus et al., 2019)

CEA with Hsap\PNPLA6^A1029T.UAS

(Sunderhaus et al., 2019)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

model of cerebellar ataxia

is ameliorated by Hsap\PNPLA6^UAS.cTa

(Topaloglu et al., 2014)

is exacerbated by Hsap\PNPLA6^F1M.UAS

(Topaloglu et al., 2014)

model of neurodegenerative disease

is exacerbated by per⁰¹

(Krishnan et al., 2012)

is ameliorated by Mmus\Xbp1^UAS.cCTa

(Sunderhaus et al., 2019)

is ameliorated by SERCA^UAS.cFa

(Sunderhaus et al., 2019)

is ameliorated by Xbp1^UAS.LG.EGFP

(Sunderhaus et al., 2019)

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

Detailed Description

Statement

Reference

sws¹ adults show a progressive decrease in locomotion in fast phototaxis assays, and barely move by day 14, when they exhibit severe vacuolization of the deutocerebral neuropil.

(Sunderhaus et al., 2019)

sws¹/sws¹ 1 day old adults show glial hyper-wrapping and incomplete glial wrapping of neuronal cell bodies and stunted glial processes in the medulla cortex.

sws¹/sws¹ flies (two days old) have a significantly reduced performance in a phototaxis assay (measuring percentage transitions towards light) compared to controls; this phenotype is progressive, with performance in 14 day old flies worse than in 2 day old flies.

(Dutta et al., 2016)

sws¹ mutant brains exhibit progressive neurodegeneration, with a significant increase in vacuole formation at 7, 14, and 21 days old, but not at 1 day old, as compared to wild type.

(Sunderhaus and Kretzschmar, 2016)

sws¹ flies shortly before eclosion have normal eyes with all photoreceptors present. Whereas 14-day-old flies still have mostly intact ommatidia (occasionally one photoreceptor is lost), at 23 days the photoreceptors are either lost or show degenerative signs such as condensed cell bodies, intracellular membranous bodies or vacuoles.

(Kmoch et al., 2015)

sws¹ flies show neurodegeneration compared to controls, with vacuoles present in the brain at 14 days of age.

(Topaloglu et al., 2014)

sws¹/+ flies do not exhibit a significant difference in performance in a phototaxis assay, as compared to controls; but both sws¹/+ and sws¹/sws¹ flies exhibit significantly increased vacuolization in the brain as compared to wild type.

(Wentzell et al., 2014)

sws¹ mutants at 14 days old do not display any marked defects in circadian rhythms, but do exhibit symptoms of neurodegeneration evidenced by vacuoles in the brain.

(Krishnan et al., 2012)

14 day old vap^KS67 mutant flies show vacuoles in all parts of the brain. These increase dramatically with age.

(Wentzell et al., 2012)

sws¹/sws¹ flies show vacuolization in the neuropil.

(Bettencourt da Cruz et al., 2008)

sws¹ flies exhibit vacuolisation in the neuropil (due to degeneration of neurites) and the formation of membranous glial bodies.

sws¹ flies exhibit a strong glial phenotype consisting of the formation of multilayered glial wrappings and subsequent glial cell death.

(Muhlig-Versen et al., 2005)

Adults have vacuoles in all brain regions. This degeneration increases with age, as shown by an increased number of vacuoles and shrinking of the cell cortex. An increasing amount of cell death is also seen in the brain. Compact dark bodies are seen in the cortex, especially the lamina cortex. These structures are first seen during late pupal stages, and increase in size during aging of the adult. Approximately 10% of brain cortex neurons are enwrapped by multilayered membranes originating from nearby glia in newly eclosed flies. Membranous whorls are seen in older flies. Homozygotes adults show a significant reduction in lifespan compared to wild-type flies.

(Kretzschmar et al., 1997)

many Swiss-cheese-like holes seen in brain sections of adults (similar to phenotype observed in dying drd flies). Phenotype has become less extreme, apparently due to accumulation of modifiers (Heisenberg).

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

sws¹ has abnormal neuroanatomy | adult stage phenotype, enhanceable by Scer\GAL4^Appl.PU/Hsap\PNPLA6^F1M.UAS

(Topaloglu et al., 2014)

sws¹ has abnormal neuroanatomy | adult stage phenotype, enhanceable by per⁰¹

(Krishnan et al., 2012)

sws¹ has abnormal neuroanatomy | adult stage phenotype, enhanceable by Scer\GAL4^Appl.G1a/Pka-C3^UAS.cBa

(Bettencourt da Cruz et al., 2008)

NOT Enhanced by

Statement

Reference

sws¹ has abnormal neuroanatomy | adult stage phenotype, non-enhanceable by Hsap\PNPLA6^F2M1.UAS/Scer\GAL4^Appl.PU

(Topaloglu et al., 2014)

sws¹ has abnormal neuroanatomy | adult stage phenotype, non-enhanceable by Hsap\PNPLA6^F2M2.UAS/Scer\GAL4^Appl.PU

(Topaloglu et al., 2014)

sws¹ has abnormal neuroanatomy | adult stage phenotype, non-enhanceable by Pka-C1[+]/Pka-C1^C2

(Bettencourt da Cruz et al., 2008)

Suppressed by

Statement

Reference

sws¹ has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible | partially by Hsap\PNPLA6^UAS.cTa/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible | partially by Hsap\PNPLA6^L524P.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible | partially by Scer\GAL4^Appl.G1a/Hsap\PNPLA6^G578W.UAS

(Sunderhaus et al., 2019)

sws¹ has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible | partially by Hsap\PNPLA6^T629R.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible | partially by Hsap\PNPLA6^A1029T.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has abnormal locomotor behavior | adult stage | progressive phenotype, suppressible | partially by Scer\GAL4^Appl.G1a/Hsap\PNPLA6^R1099Q.UAS

(Sunderhaus et al., 2019)

sws¹ has abnormal neuroanatomy | adult stage phenotype, suppressible | partially by Hsap\PNPLA6^UAS.cTa/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has abnormal neuroanatomy | adult stage phenotype, suppressible | partially by Scer\GAL4^Appl.G1a/Hsap\PNPLA6^R1099Q.UAS

(Sunderhaus et al., 2019)

sws¹ has abnormal neuroanatomy | adult stage phenotype, suppressible | partially by Hsap\PNPLA6^A1029T.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has abnormal neuroanatomy | adult stage phenotype, suppressible | partially by Scer\GAL4^Appl.G1a/Hsap\PNPLA6^G578W.UAS

(Sunderhaus et al., 2019)

sws¹ has abnormal neuroanatomy | adult stage phenotype, suppressible | partially by Hsap\PNPLA6^L524P.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has abnormal neuroanatomy | adult stage phenotype, suppressible | partially by Hsap\PNPLA6^UAS.cTa/Scer\GAL4^Appl.PU

(Topaloglu et al., 2014)

sws¹ has abnormal neuroanatomy | adult stage phenotype, suppressible by Scer\GAL4^elav-C155/Appl^s.UAS.Tag:HA

(Wentzell et al., 2012)

sws¹ has abnormal neuroanatomy | adult stage phenotype, suppressible by Scer\GAL4^elav-C155/Appl^UAS.cCSa

(Wentzell et al., 2012)

sws¹ has abnormal neuroanatomy | adult stage phenotype, suppressible | partially by +/Df(3L)brm11

(Bettencourt da Cruz et al., 2008)

sws¹ has abnormal neuroanatomy phenotype, suppressible by Scer\GAL4^elav-C155/Mmus\Pnpla6^UAS.cMa

(Muhlig-Versen et al., 2005)

sws¹ has abnormal neuroanatomy phenotype, suppressible by Scer\GAL4^loco.1.3/Mmus\Pnpla6^UAS.cMa

(Muhlig-Versen et al., 2005)

NOT suppressed by

Statement

Reference

sws¹ has abnormal locomotor behavior | adult stage | progressive phenotype, non-suppressible by Hsap\PNPLA6^F2M1.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has abnormal neuroanatomy | adult stage phenotype, non-suppressible by Hsap\PNPLA6^F2M1.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has abnormal neuroanatomy | adult stage phenotype, non-suppressible by Hsap\PNPLA6^T629R.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has abnormal neuroanatomy | adult stage phenotype, non-suppressible by Hsap\PNPLA6^F2M1.UAS/Scer\GAL4^Appl.PU

(Topaloglu et al., 2014)

sws¹ has abnormal neuroanatomy | adult stage phenotype, non-suppressible by Hsap\PNPLA6^F2M2.UAS/Scer\GAL4^Appl.PU

(Topaloglu et al., 2014)

Enhancer of

Statement

Reference

sws[+]/sws¹ is an enhancer of abnormal neuroanatomy | adult stage | male | progressive phenotype of Pka-C3^UAS.cBa, Scer\GAL4^Appl.G1a

(Bettencourt da Cruz et al., 2008)

Other

Statement

Reference

per⁰¹, sws¹ has abnormal circadian rhythm phenotype

(Krishnan et al., 2012)

Pka-C3^UAS.cBa, Scer\GAL4^Appl.G1a, sws[+]/sws¹ has abnormal neuroanatomy | female | adult stage | progressive phenotype

(Bettencourt da Cruz et al., 2008)

Phenotype Manifest In

Enhanced by

Statement

Reference

sws¹ has adult brain phenotype, enhanceable by Scer\GAL4^Appl.PU/Hsap\PNPLA6^F1M.UAS

(Topaloglu et al., 2014)

sws¹ has vacuole phenotype, enhanceable by per⁰¹

(Krishnan et al., 2012)

sws¹ has adult brain phenotype, enhanceable by per⁰¹

(Krishnan et al., 2012)

sws¹ has neuropil | adult stage phenotype, enhanceable by Scer\GAL4^Appl.G1a/Pka-C3^UAS.cBa

(Bettencourt da Cruz et al., 2008)

NOT Enhanced by

Statement

Reference

sws¹ has adult brain phenotype, non-enhanceable by Hsap\PNPLA6^F2M1.UAS/Scer\GAL4^Appl.PU

(Topaloglu et al., 2014)

sws¹ has adult brain phenotype, non-enhanceable by Hsap\PNPLA6^F2M2.UAS/Scer\GAL4^Appl.PU

(Topaloglu et al., 2014)

sws¹ has neuropil | adult stage phenotype, non-enhanceable by Pka-C1[+]/Pka-C1^C2

(Bettencourt da Cruz et al., 2008)

Suppressed by

Statement

Reference

sws¹ has adult deutocerebrum phenotype, suppressible | partially by Hsap\PNPLA6^UAS.cTa/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has adult deutocerebrum phenotype, suppressible | partially by Hsap\PNPLA6^A1029T.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has adult deutocerebrum phenotype, suppressible | partially by Scer\GAL4^Appl.G1a/Hsap\PNPLA6^R1099Q.UAS

(Sunderhaus et al., 2019)

sws¹ has adult deutocerebrum phenotype, suppressible | partially by Scer\GAL4^Appl.G1a/Hsap\PNPLA6^G578W.UAS

(Sunderhaus et al., 2019)

sws¹ has adult deutocerebrum phenotype, suppressible | partially by Hsap\PNPLA6^L524P.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has adult brain phenotype, suppressible | partially by Hsap\PNPLA6^UAS.cTa/Scer\GAL4^Appl.PU

(Topaloglu et al., 2014)

sws¹ has adult brain phenotype, suppressible by Scer\GAL4^elav-C155/Appl^s.UAS.Tag:HA

(Wentzell et al., 2012)

sws¹ has adult brain phenotype, suppressible by Scer\GAL4^elav-C155/Appl^UAS.cCSa

(Wentzell et al., 2012)

sws¹ has lamina phenotype, suppressible | partially by +/Df(3L)brm11

(Bettencourt da Cruz et al., 2008)

sws¹ has neuropil phenotype, suppressible by Scer\GAL4^elav-C155/Mmus\Pnpla6^UAS.cMa

(Muhlig-Versen et al., 2005)

sws¹ has CNS glial cell phenotype, suppressible by Scer\GAL4^elav-C155/Mmus\Pnpla6^UAS.cMa

(Muhlig-Versen et al., 2005)

sws¹ has CNS glial cell phenotype, suppressible by Scer\GAL4^loco.1.3/Mmus\Pnpla6^UAS.cMa

(Muhlig-Versen et al., 2005)

NOT suppressed by

Statement

Reference

sws¹ has adult deutocerebrum phenotype, non-suppressible by Hsap\PNPLA6^F2M1.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has adult deutocerebrum phenotype, non-suppressible by Hsap\PNPLA6^T629R.UAS/Scer\GAL4^Appl.G1a

(Sunderhaus et al., 2019)

sws¹ has adult brain phenotype, non-suppressible by Hsap\PNPLA6^F2M1.UAS/Scer\GAL4^Appl.PU

(Topaloglu et al., 2014)

sws¹ has adult brain phenotype, non-suppressible by Hsap\PNPLA6^F2M2.UAS/Scer\GAL4^Appl.PU

(Topaloglu et al., 2014)

sws¹ has adult cerebrum phenotype, non-suppressible by +/Df(3L)brm11

(Bettencourt da Cruz et al., 2008)

Enhancer of

Statement

Reference

sws[+]/sws¹ is an enhancer of neuropil | adult stage | male | progressive phenotype of Pka-C3^UAS.cBa, Scer\GAL4^Appl.G1a

(Bettencourt da Cruz et al., 2008)

Other

Statement

Reference

Pka-C3^UAS.cBa, Scer\GAL4^Appl.G1a, sws[+]/sws¹ has neuropil | female | adult stage | progressive phenotype

(Bettencourt da Cruz et al., 2008)

Additional Comments

Genetic Interactions

Statement

Reference

per⁰¹, sws¹ double mutants at 14 days old show marked increase in neurodegeneration as measured by area and number of vacuoles in the brain as compared to sws¹ single mutants.

A subset of per⁰¹, sws¹ double mutants exhibit some rhythmicity (13% of flies), in contrast to per⁰¹ single mutants in which 0% of flies have circadian rhythm, and sws¹ single mutants in which 97% of flies have circadian rhythm.

(Krishnan et al., 2012)

Expression of Appl^{s.Scer\UAS.T:Ivir\HA1} under the control of Scer\GAL4^elav-C155 fails to suppress the vacuolisation seen in the brains of sws¹ mutant 14 day old males.

Expression of Appl^{Scer\UAS.cCSa} under the control of Scer\GAL4^elav-C155 fails to suppress the vacuolisation seen in the brains of sws¹ mutant 14 day old males.

(Wentzell et al., 2012)

Expression of Pka-C3^Scer\UAS.cBa driven pan-neuronally by Scer\GAL4^Appl.G1a enhances neuropil vacuolization in sws¹/sws¹ flies. Df(3L)brm11/+ partially suppresses neuropil vacuolization in the lamina cortex (but not central brain) of sws¹/sws¹ flies. Pka-C1^C2/+ does not enhance vacuole formation in sws¹/sws¹ flies.

sws¹/+ enhances degeneration (neuropil vacuolization) in aged male flies with expression of Pka-C3^Scer\UAS.cBa driven pan-neuronally by Scer\GAL4^Appl.G1a, and also results in vacuolization in aged females.

(Bettencourt da Cruz et al., 2008)

Xenogenetic Interactions

Statement

Reference

Expression of Hsap\PNPLA6^Scer\UAS.cTa driven by Scer\GAL4^Appl.PU significantly partially suppresses neurodegeneration (vacuoles in the brain) in 14 day old sws¹ flies. Expression of Hsap\PNPLA6^F1M.Scer\UAS driven by Scer\GAL4^Appl.PU significantly enhances neurodegeneration sws¹ flies. Expression of Hsap\PNPLA6^{F2M1.Scer\UAS} or Hsap\PNPLA6^{F2M2.Scer\UAS} driven by Scer\GAL4^Appl.PU does not affect neurodegeneration sws¹ flies.

(Topaloglu et al., 2014)

Neuronal expression of Mmus\NTE^Scer\UAS.cMa, under the control of Scer\GAL4^elav-C155 rescues some aspects of the neuronal degeneration, namely the vacuolisation in the neuropil.

Glial expression of Mmus\NTE^Scer\UAS.cMa, under the control of Scer\GAL4^loco.1.3 rescues the glial phenotype.

Expression of Mmus\NTE^Scer\UAS.cMa in either neurons or glia (under the control of either Scer\GAL4^elav-C155 or Scer\GAL4^loco.1.3) restores the wild-type NTE-like activity (NTE-neuropathy target esterase).

(Muhlig-Versen et al., 2005)

Complementation and Rescue Data

Complements

sws^olfE-x26

(Kretzschmar et al., 1997)

Rescued by

sws¹ is rescued by sws^UAS.cMa/Scer\GAL4^elav-C155

(Muhlig-Versen et al., 2005)

sws¹ is rescued by sws^UAS.cMa/Scer\GAL4^loco.1.3

(Muhlig-Versen et al., 2005)

Partially rescued by

sws¹ is partially rescued by sws^UAS.cMa/Scer\GAL4^loco.PU

(Dutta et al., 2016)

sws¹ is partially rescued by sws^UAS.cMa/Scer\GAL4^elav.PU

(Dutta et al., 2016)

sws¹ is partially rescued by Scer\GAL4^Appl.G1a/sws^R133A.UAS

(Bettencourt da Cruz et al., 2008)

sws¹ is partially rescued by sws^UAS.cMa/Scer\GAL4^Appl.G1a

(Bettencourt da Cruz et al., 2008)

sws¹ is partially rescued by sws^S985D.UAS/Scer\GAL4^Appl.G1a

(Bettencourt da Cruz et al., 2008)

Not rescued by

sws¹ is not rescued by Scer\GAL4^elav-C155/sws^S985D.UAS

(Muhlig-Versen et al., 2005)

sws¹ is not rescued by Scer\GAL4^loco.1.3/sws^S985D.UAS

(Muhlig-Versen et al., 2005)

Comments

Expression of sws^Scer\UAS.cMa driven by Scer\GAL4^loco.PU partially restores glial wrapping of neuronal cell bodies in the medulla cortex and neurites in the medulla neuropil in sws¹/sws¹ flies, though some vacuoles are still present (glial hyper-wrapping no longer occurs).

Scer\GAL4^elav.PU>sws^Scer\UAS.cMa flies still show incomplete glial wrapping in the medulla, though glial sheaths are present in some neuronal cell bodies in the medulla cortex and neurites in the medulla neuropil in sws¹/sws¹ flies (glial hyper-wrapping no longer occurs).

(Dutta et al., 2016)

Expression of sws^{R133A.Scer\UAS} driven pan-neuronally by Scer\GAL4^Appl.G1a significantly (partially) rescues neuropil vacuolization in sws¹/sws¹ flies, though this rescue is significantly less than is seen with expression of sws^Scer\UAS.cMa (almost full rescue). Expression of sws^{S985D.Scer\UAS} driven pan-neuronally by Scer\GAL4^Appl.G1a partially rescues neuropil vacuolization in sws¹/sws¹ flies (though this rescue is less than is seen with expression of sws^Scer\UAS.cMa).

(Bettencourt da Cruz et al., 2008)

Neuronal expression of sws^Scer\UAS.cMa, under the control of Scer\GAL4^elav-C155 rescues some aspects of sws¹ neuronal degeneration, namely the vacuolisation in the neuropil.

Glial expression of sws^Scer\UAS.cMa, under the control of Scer\GAL4^loco.1.3 rescues the glial phenotype found in sws¹ mutants.

Expression of sws^Scer\UAS.cMa in either neurons or glia (under the control of either Scer\GAL4^elav-C155 or Scer\GAL4^loco.1.3) restores the wild-type NTE-like activity (NTE-neuropathy target esterase).

(Muhlig-Versen et al., 2005)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Heisenberg.

Selected as: Anatomical defect (see FBrf0033934).

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

HK151

sws¹

(Melentev et al., 2021, Melentev et al., 2021, Sunderhaus et al., 2019, Sunderhaus et al., 2019, Dutta et al., 2016, Sunderhaus and Kretzschmar, 2016, Kmoch et al., 2015, Topaloglu et al., 2014, Wentzell et al., 2014, Krishnan et al., 2012, Wentzell et al., 2012, Bettencourt da Cruz et al., 2008, Muhlig-Versen et al., 2005)

Name Synonyms

Secondary FlyBase IDs

References (14)

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