FlyBase Allele Report: Dmel\Atg18a[Δ585]

General Information

Symbol

Dmel\Atg18a^Δ585

Species

D. melanogaster

Name

FlyBase ID

FBal0263634

Feature type

allele

Associated gene

Dmel\Atg18a

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Shen and Ganetzky, 2009)

Progenitor genotype

Cytology

Description

Imprecise excision of P{SUPor-P}Atg18^KG03090, found 127bp upstream of the ATG start codon, deletes 585bp downstream of the P{SUPor-P}Atg18^KG03090 insertion site, removing the second exon, including the strt codon, and part of the third exon.

(Shen and Ganetzky, 2009)

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 ( 0 )

Disease

Evidence

References

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 neuroanatomy

(Shen and Ganetzky, 2009)

decreased cell growth rate

(Shen and Ganetzky, 2009)

Phenotype Manifest In

neuromuscular junction

(Shen and Ganetzky, 2009)

NMJ bouton

(Shen and Ganetzky, 2009)

Detailed Description

Statement

Reference

Atg18^Δ585/+ mutants exhibit a neuromuscular junction undergrowth phenotype but do not exhibit defects in axonal transport.

A Atg18^Δ585 heterozygous background has no effect on neuromuscular junction growth in an otherwise wild-type background.

A Atg18^Δ585 heterozygous background completely suppresses rapamycin-induced neuromuscular junction overgrowth.

(Shen and Ganetzky, 2009)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressor of

Statement

Reference

Atg18a^Δ585/Atg18[+] is a suppressor of abnormal neuroanatomy phenotype of Atg1^UAS.cSa, Scer\GAL4^elav.PLu

(Shen and Ganetzky, 2009)

Atg18a^Δ585/Atg18[+] is a suppressor of increased cell growth rate phenotype of Atg1^UAS.cSa, Scer\GAL4^elav.PLu

(Shen and Ganetzky, 2009)

Atg18a^Δ585 is a suppressor of abnormal neuroanatomy phenotype of Atg1^UAS.cSa, Scer\GAL4^elav.PLu

(Shen and Ganetzky, 2009)

Atg18a^Δ585 is a suppressor of increased cell growth rate phenotype of Atg1^UAS.cSa, Scer\GAL4^elav.PLu

(Shen and Ganetzky, 2009)

Phenotype Manifest In

Suppressor of

Statement

Reference

Atg18a^Δ585/Atg18[+] is a suppressor of NMJ bouton phenotype of Atg1^UAS.cSa, Scer\GAL4^elav.PLu

(Shen and Ganetzky, 2009)

Atg18a^Δ585/Atg18[+] is a suppressor of neuromuscular junction phenotype of Atg1^UAS.cSa, Scer\GAL4^elav.PLu

(Shen and Ganetzky, 2009)

Atg18a^Δ585 is a suppressor of NMJ bouton phenotype of Atg1^UAS.cSa, Scer\GAL4^elav.PLu

(Shen and Ganetzky, 2009)

Atg18a^Δ585 is a suppressor of neuromuscular junction phenotype of Atg1^UAS.cSa, Scer\GAL4^elav.PLu

(Shen and Ganetzky, 2009)

Additional Comments

Genetic Interactions

Statement

Reference

A Atg18^Δ585 heterozygous background significantly suppresses neuromuscular junction overgrowth caused by neuronal expression of Atg1^Scer\UAS.cSa under the control of Scer\GAL4^elav.PLu. Removal of both copies of Atg18 confers almost complete suppression.

(Shen and Ganetzky, 2009)

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 (3)

Reported As

Symbol Synonym

Atg18^Δ585

Atg18a^Δ585

atg18^Δ

(Shen and Ganetzky, 2009)

Name Synonyms

Secondary FlyBase IDs

References (1)

Report Sections

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