FlyBase Allele Report: Dmel\Rab7[Gal4-KO]

General Information

Symbol

Dmel\Rab7^Gal4-KO

Species

D. melanogaster

Name

FlyBase ID

FBal0294205

Feature type

allele

Associated gene

Dmel\Rab7

Associated Insertion(s)

TI{GAL4}Rab7^Gal4-KO

Carried in Construct

Also Known As

rab7^{Gal4-knock-in}

Key Links

Allele class

amorphic allele - molecular evidence

Mutagen

ends-out gene targeting

Nature of the Allele

Allele class

amorphic allele - molecular evidence

(Cherry et al., 2013)

Mutagen

ends-out gene targeting

(Cherry et al., 2013)

Progenitor genotype

Associated Insertion(s)

TI{GAL4}Rab7^Gal4-KO

Cytology

Description

The Rab7 open reading frame has been replaced by a cassette containing sequence encoding a GAL4 driver and a Disc\RFP^3xP3.PC marker.

(Cherry et al., 2013)

Allele components

Component

Use(s)

Inserted element

TI{GAL4}

promoter trap

Encoded product / tool

GAL4

binary expression system - driver

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 Charcot-Marie-Tooth disease type 2

CEA

(Cherry et al., 2013)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

ameliorates amyotrophic lateral sclerosis type 8

modeled by Vap33^Δ20

(Mao et al., 2019)

ameliorates autosomal dominant adult-onset proximal spinal muscular atrophy

modeled by Vap33^Δ20

(Mao et al., 2019)

exacerbates Alzheimer's disease 1

modeled by Appl^d

(Kessissoglou et al., 2020)

exacerbates amyotrophic lateral sclerosis type 10

modeled by Hsap\TARDBP^UAS.cUa

(Liu et al., 2017)

modeled by Hsap\TARDBP^G298S.UAS

(Liu et al., 2017)

Comments on Models/Modifiers Based on Experimental Evidence ( 1 )

The Charcot-Marie-Tooth 2B disease is a genetically dominant disorder as all patients contain one wild-type copy and one mutant copy of the human Hsap\RAB7A gene. It has been proposed that the mutant forms of Hsap\RAB7A that are seen in Charcot-Marie-Tooth 2B disease patients are gain of function mutations which cause the adult onset neurodegeneration characteristic of the disease. However, studies in a Drosophila model suggest that the neurodegeneration seen in Charcot-Marie-Tooth 2B disease may be caused by loss of normal Hsap\RAB7A function in the patients rather than by the presence of the mutant protein: mutant flies that completely lack function of the Drosophila Rab7 gene in the eye show adult onset neurodegeneration, while flies overexpressing mutant forms of Rab7 which have been identified in Charcot-Marie-Tooth 2B disease patients (the flies express either a mutant form of Hsap\RAB7A or express the equivalent mutations in the Drosophila Rab7 ortholog) do not show neurodegeneration.

(Cherry et al., 2013)

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

photoreceptor

(Cherry et al., 2013)

photoreceptor | progressive | somatic clone

(Cherry et al., 2013)

rhabdomere

(Cherry et al., 2013)

rhabdomere | progressive | somatic clone

(Cherry et al., 2013)

synapse

(Cherry et al., 2013)

synapse | progressive | somatic clone

(Cherry et al., 2013)

Detailed Description

Statement

Reference

Rab7^{GAL4.T:Disc\RFP} mutant flies result in lethality at between 50 and 80% of pupal lethality, with no gross morphological abnormalities. Loss of maternal Rab7 causes lethality in fully developed embryos with no obvious developmental defects. Overall brain structure appears normal, and photoreceptor specification and axon path-finding are comparable to wild type.

Eyes composed entirely of Rab7^{GAL4.T:Disc\RFP} mutant photoreceptor cells (generated using eyFLP) appear morphologically normal.

Electroretinogram recordings reveal no defects in the amplitudes of light-evoked responses and synaptic function in Rab7^{GAL4.T:Disc\RFP} mutant eye clones in newly eclosed adults. However by 5 days old, flies raised in constant ambient light show almost complete loss of synaptic function, a phenotype that is not observed in wild type flies. This loss of synaptic function can be fully rescued by raising the flies in the dark. The light-evoked response amplitude remains unchanged in these flies.

The photoreceptors of Rab7^{GAL4.T:Disc\RFP} mutant eye clones in 5 day old flies raised in the light exhibit rhabdomere degeneration and vacuolisation and degeneration of synaptic terminals. This is not seen in either controls or Rab7^{GAL4.T:Disc\RFP} mutant flies raised in the dark.

Electroretinogram recordings from the larval neuromuscular junction of the Rab7^{GAL4.T:Disc\RFP} mutant are indistinguishable from wild type. The frequency and amplitudes of spontaneous single vesicle release events are normal, as are evoked neurotransmission events.

Flies expressing one copy of Rab7^{Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of one copy of Scer\GAL4^{Rab7.T:Disc\RFP} (in a Rab7^{GAL4.T:Disc\RFP}/+ mutant background) are viable and do not display any obvious behavioural defects or altered lifespan. Electroretinogram recordings from the larval neuromuscular junction are indistinguishable from wild type. The frequency and amplitudes of spontaneous single vesicle release events are normal, as are evoked neurotransmission events. As in wild type, no photoreceptor defects, either morphological or functional, are seen in adult flies that have been exposed to 10 days of constant light stimulation.

Flies expressing one copy of Rab7^{Q67L.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of one copy of Scer\GAL4^{Rab7.T:Disc\RFP} (in a Rab7^{GAL4.T:Disc\RFP}/+ mutant background) are viable and do not display any obvious behavioural defects or altered lifespan. Electroretinogram recordings from the larval neuromuscular junction are indistinguishable from wild type. The frequency and amplitudes of spontaneous single vesicle release events are normal, as are evoked neurotransmission events. As in wild type, no photoreceptor defects, either morphological or functional, are seen in adult flies that have been exposed to 10 days of constant light stimulation.

Flies expressing one copy of Rab7^{T22N.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of one copy of Scer\GAL4^{Rab7.T:Disc\RFP} (in a Rab7^{GAL4.T:Disc\RFP}/+ mutant background) are viable and do not display any obvious behavioural defects or altered lifespan. Electroretinogram recordings from the larval neuromuscular junction are indistinguishable from wild type. The frequency and amplitudes of spontaneous single vesicle release events are normal, as are evoked neurotransmission events. As in wild type, no photoreceptor defects, either morphological or functional, are seen in adult flies that have been exposed to 10 days of constant light stimulation.

Flies expressing one copy of Rab7^{K157N.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of one copy of Scer\GAL4^{Rab7.T:Disc\RFP} (in a Rab7^{GAL4.T:Disc\RFP}/+ mutant background) are viable and do not display any obvious behavioural defects or altered lifespan. Electroretinogram recordings from the larval neuromuscular junction are indistinguishable from wild type. The frequency and amplitudes of spontaneous single vesicle release events are normal, as are evoked neurotransmission events. As in wild type, no photoreceptor defects, either morphological or functional, are seen in adult flies that have been exposed to 10 days of constant light stimulation.

Flies expressing one copy of Rab7^{L129F.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of one copy of Scer\GAL4^{Rab7.T:Disc\RFP} (in a Rab7^{GAL4.T:Disc\RFP}/+ mutant background) are viable and do not display any obvious behavioural defects or altered lifespan. Electroretinogram recordings from the larval neuromuscular junction are indistinguishable from wild type. The frequency and amplitudes of spontaneous single vesicle release events are normal, as are evoked neurotransmission events. As in wild type, no photoreceptor defects, either morphological or functional, are seen in adult flies that have been exposed to 10 days of constant light stimulation.

Flies expressing Rab7^{N161T.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of one copy of Scer\GAL4^{Rab7.T:Disc\RFP} (in a Rab7^{GAL4.T:Disc\RFP}/+ mutant background) are viable and do not display any obvious behavioural defects or altered lifespan. Electroretinogram recordings from the larval neuromuscular junction are indistinguishable from wild type. The frequency and amplitudes of spontaneous single vesicle release events are normal, as are evoked neurotransmission events. As in wild type, no photoreceptor defects, either morphological or functional, are seen in adult flies that have been exposed to 10 days of constant light stimulation.

Flies expressing one copy of Rab7^{V162M.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of one copy of Scer\GAL4^{Rab7.T:Disc\RFP} (in a Rab7^{GAL4.T:Disc\RFP}/+ mutant background) are viable and do not display any obvious behavioural defects or altered lifespan. Electroretinogram recordings from the larval neuromuscular junction are indistinguishable from wild type. The frequency and amplitudes of spontaneous single vesicle release events are normal, as are evoked neurotransmission events. As in wild type, no photoreceptor defects, either morphological or functional, are seen in adult flies that have been exposed to 10 days of constant light stimulation.

Defects in synaptic function defects are seen in heterozygous Rab7^{GAL4.T:Disc\RFP} mutant flies that have been raised in constant light for 10 days. The phenotype is not present when flies are raised in the dark and the light-evoked response amplitude is unaffected. Partial loss of rhabdomere structures is seen when heterozygous flies are raised in constant light for either 5 and 10 days.

(Cherry et al., 2013)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Rab7^Gal4-KO has abnormal neuroanatomy | somatic clone | adult stage | progressive phenotype, suppressible by Scer\GAL4^Rab7-Gal4-KO/Hsap\RAB7A^{K157N.UAS.Venus}

(Cherry et al., 2013)

Rab7^Gal4-KO has abnormal neurophysiology | dominant phenotype, suppressible by Scer\GAL4^Rab7-Gal4-KO/Hsap\RAB7A^UAS.Venus

(Cherry et al., 2013)

Rab7^Gal4-KO has lethal - all die before end of pupal stage | recessive phenotype, suppressible by Scer\GAL4^Rab7-Gal4-KO/Hsap\RAB7A^UAS.Venus

(Cherry et al., 2013)

Rab7^Gal4-KO has abnormal neurophysiology | somatic clone | adult stage | progressive phenotype, suppressible by Scer\GAL4^Rab7-Gal4-KO/Hsap\RAB7A^UAS.Venus

(Cherry et al., 2013)

Rab7^Gal4-KO has abnormal neuroanatomy | somatic clone | adult stage | progressive phenotype, suppressible by Scer\GAL4^Rab7-Gal4-KO/Hsap\RAB7A^UAS.Venus

(Cherry et al., 2013)

Rab7^Gal4-KO has abnormal neurophysiology | dominant phenotype, suppressible by Scer\GAL4^Rab7-Gal4-KO/Hsap\RAB7A^{K157N.UAS.Venus}

(Cherry et al., 2013)

Rab7^Gal4-KO has lethal - all die before end of pupal stage | recessive phenotype, suppressible by Scer\GAL4^Rab7-Gal4-KO/Hsap\RAB7A^{K157N.UAS.Venus}

(Cherry et al., 2013)

Rab7^Gal4-KO has abnormal neurophysiology | somatic clone | adult stage | progressive phenotype, suppressible by Scer\GAL4^Rab7-Gal4-KO/Hsap\RAB7A^{K157N.UAS.Venus}

(Cherry et al., 2013)

Suppressor of

Statement

Reference

Rab7[+]/Rab7^Gal4-KO is a suppressor of abnormal locomotor behavior | adult stage | progressive phenotype of Df(2L)Exel6004/Vps29¹

(Ye et al., 2020)

Rab7[+]/Rab7^Gal4-KO is a suppressor | partially of abnormal neurophysiology | adult stage phenotype of Df(2L)Exel6004/Vps29¹

(Ye et al., 2020)

Other

Statement

Reference

Hsap\RAB7A^UAS.Venus, Rab7^Gal4-KO, Scer\GAL4^Rab7-Gal4-KO has viable phenotype

(Cherry et al., 2013)

Hsap\RAB7A^{K157N.UAS.Venus}, Rab7^Gal4-KO, Scer\GAL4^Rab7-Gal4-KO has viable phenotype

(Cherry et al., 2013)

Phenotype Manifest In

Suppressor of

Statement

Reference

Rab7[+]/Rab7^Gal4-KO is a suppressor | partially of retina | adult stage phenotype of Df(2L)Exel6004/Vps29¹

(Ye et al., 2020)

Additional Comments

Genetic Interactions

Statement

Reference

Xenogenetic Interactions

Statement

Reference

Flies expressing one copy of Hsap\RAB7A^{Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of one copy of Scer\GAL4^{Rab7.T:Disc\RFP} (in a Rab7^{GAL4.T:Disc\RFP}/+ mutant background) are viable and do not display any obvious behavioural defects or altered lifespan. Electroretinogram recordings from the larval neuromuscular junction are indistinguishable from wild type. The frequency and amplitudes of spontaneous single vesicle release events are normal, as are evoked neurotransmission events. As in wild type, no photoreceptor defects, either morphological or functional, are seen in adult flies that have been exposed to 10 days of constant light stimulation.

Expression of one copy of Hsap\RAB7A^{Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the lethality seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant flies.

Expression of Hsap\RAB7A^{Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} partially rescues the progressive synaptic and neuronal degeneration seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant eye clones after 10 days of constant light stimulation.

Flies expressing Hsap\RAB7A^{K157N.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of one copy of Scer\GAL4^{Rab7.T:Disc\RFP} (in a Rab7^{GAL4.T:Disc\RFP}/+ mutant background) are viable and do not display any obvious behavioural defects or altered lifespan. Electroretinogram recordings from the larval neuromuscular junction are indistinguishable from wild type. The frequency and amplitudes of spontaneous single vesicle release events are normal, as are evoked neurotransmission events. As in wild type, no photoreceptor defects, either morphological or functional, are seen in adult flies that have been exposed to 10 days of constant light stimulation.

Expression of Hsap\RAB7A^{K157N.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the lethality seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant flies.

Expression of Hsap\RAB7A^{K157N.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} partially rescues the progressive synaptic and neuronal degeneration seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant eye clones after 10 days of constant light stimulation.

(Cherry et al., 2013)

Complementation and Rescue Data

Rescued by

[+]/Rab7^Gal4-KO is rescued by Rab7^UAS.Venus/Scer\GAL4^Rab7-Gal4-KO

(Cherry et al., 2013)

[+]/Rab7^Gal4-KO is rescued by Scer\GAL4^Rab7-Gal4-KO/Rab7^{L129F.UAS.Venus}

(Cherry et al., 2013)

[+]/Rab7^Gal4-KO is rescued by Scer\GAL4^Rab7-Gal4-KO/Rab7^{K157N.UAS.Venus}

(Cherry et al., 2013)

[+]/Rab7^Gal4-KO is rescued by Scer\GAL4^Rab7-Gal4-KO/Rab7^{N161T.UAS.Venus}

(Cherry et al., 2013)

[+]/Rab7^Gal4-KO is rescued by Rab7^{V162M.UAS.Venus}/Scer\GAL4^Rab7-Gal4-KO

(Cherry et al., 2013)

Rab7^Gal4-KO is rescued by Scer\GAL4^Rab7-Gal4-KO/Rab7^{Q67L.UAS.Venus}

(Cherry et al., 2013)

Rab7^Gal4-KO is rescued by Rab7^UAS.Venus/Scer\GAL4^Rab7-Gal4-KO

(Cherry et al., 2013)

Rab7^Gal4-KO is rescued by Scer\GAL4^Rab7-Gal4-KO/Rab7^{L129F.UAS.Venus}

(Cherry et al., 2013)

Rab7^Gal4-KO is rescued by Scer\GAL4^Rab7-Gal4-KO/Rab7^{K157N.UAS.Venus}

(Cherry et al., 2013)

Rab7^Gal4-KO is rescued by Scer\GAL4^Rab7-Gal4-KO/Rab7^{N161T.UAS.Venus}

(Cherry et al., 2013)

Rab7^Gal4-KO is rescued by Rab7^{V162M.UAS.Venus}/Scer\GAL4^Rab7-Gal4-KO

(Cherry et al., 2013)

Partially rescued by

Rab7^Gal4-KO is partially rescued by Scer\GAL4^Rab7-Gal4-KO/Rab7^{T22N.UAS.Venus}

(Cherry et al., 2013)

Comments

Expression of Rab7^{Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the lethality seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant flies.

Expression of Rab7^{Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the progressive synaptic and neuronal degeneration seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant eye clones after 10 days of constant light stimulation.

Expression of Rab7^{Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the dominant defects in synaptic function and rhabdomere structure seen in Rab7^{GAL4.T:Disc\RFP}/+ mutant adults after 5 days of constant light stimulation. A similar level of rescue is seen whether the transgene expresses 0.5x, 1x or >10x the amount of endogenous Rab7 protein.

Expression of Rab7^{T22N.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} fails to rescue the lethality seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant flies. Occasional escapers are seen, but these die shortly after emergence.

Expression of Rab7^{T22N.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} partially rescues the progressive synaptic and neuronal degeneration seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant eye clones after 10 days of constant light stimulation.

Expression of Rab7^{Q67L.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the lethality seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant flies.

Expression of Rab7^{Q67L.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the progressive synaptic and neuronal degeneration seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant eye clones after 10 days of constant light stimulation.

Expression of Rab7^{K157N.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the lethality seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant flies.

Expression of Rab7^{K157N.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the progressive synaptic and neuronal degeneration seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant eye clones after 10 days of constant light stimulation.

Expression of Rab7^{K157N.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the dominant defects in synaptic function and rhabdomere structure seen in Rab7^{GAL4.T:Disc\RFP}/+ mutant adults after 5 days of constant light stimulation. A similar level of rescue is seen whether the transgene expresses 0.5x, 1x or >10x the amount of endogenous Rab7 protein.

Expression of Rab7^{L129F.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the lethality seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant flies.

Expression of Rab7^{L129F.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the progressive synaptic and neuronal degeneration seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant eye clones after 10 days of constant light stimulation.

Expression of Rab7^{L129F.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the dominant defects in synaptic function and rhabdomere structure seen in Rab7^{GAL4.T:Disc\RFP}/+ mutant adults after 5 days of constant light stimulation. A similar level of rescue is seen whether the transgene expresses 0.5x, 1x or >10x the amount of endogenous Rab7 protein.

Expression of Rab7^{N161T.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the lethality seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant flies.

Expression of Rab7^{N161T.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the progressive synaptic and neuronal degeneration seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant eye clones after 10 days of constant light stimulation.

Expression of Rab7^{N161T.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the dominant defects in synaptic function and rhabdomere structure seen in Rab7^{GAL4.T:Disc\RFP}/+ mutant adults after 5 days of constant light stimulation. A similar level of rescue is seen whether the transgene expresses 0.5x, 1x or >10x the amount of endogenous Rab7 protein.

Expression of Rab7^{V162M.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the lethality seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant flies.

Expression of Rab7^{V162M.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the progressive synaptic and neuronal degeneration seen in homozygous Rab7^{GAL4.T:Disc\RFP} mutant eye clones after 10 days of constant light stimulation.

Expression of Rab7^{V162M.Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^{Rab7.T:Disc\RFP} rescues the dominant defects in synaptic function and rhabdomere structure seen in Rab7^{GAL4.T:Disc\RFP}/+ mutant adults after 5 days of constant light stimulation. A similar level of rescue is seen whether the transgene expresses 0.5x, 1x or >10x the amount of endogenous Rab7 protein.

(Cherry et al., 2013)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (7)

Reported As

Symbol Synonym

Rab7^{GAL4.T:Disc\RFP}

Rab7^Gal4-KO

(Kohrs et al., 2021, Ye et al., 2020)

Rab7^{Gal4-knock-in}

(Tanasic et al., 2022)

Rab7^KO

(Mao et al., 2019)

Rab7KO

(Liu et al., 2017)

rab7^{Gal4-knock-in}

(Mao et al., 2019, Cherry et al., 2013)

rab7^{gal4-knock-in}

(Jin et al., 2018)

Name Synonyms

Secondary FlyBase IDs

References (11)

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