FlyBase Allele Report: Dmel\Atg1[3]

General Information

Symbol

Dmel\Atg1³

Species

D. melanogaster

Name

FlyBase ID

FBal0220537

Feature type

allele

Associated gene

Dmel\Atg1

Associated Insertion(s)

Carried in Construct

Also Known As

unc-51³

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

Mutagen

Nature of the Allele

Allele class

loss of function allele

(Toda et al., 2008)

Mutagen

Delta2-3 transposase

(Wairkar et al., 2009)

P-element activity

(Toda et al., 2008)

Progenitor genotype

Atg1^EP3348

(Wairkar et al., 2009, Toda et al., 2008)

Cytology

Description

Imprecise excision of P{EP}Atg1^EP3348has deleted 804bp downstream from the insertion point.

(Wairkar et al., 2009)

Imprecise excision of the insertion in Atg1^EP3348, resulting in a deletion of 804bp downstream from the insertion point.

(Toda et al., 2008)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

3L:12,804,179..12,804,983 [-]

Comment:

Imprecise excision of the P{EP}Atg1^EP3348 insertion resulting in a deletion that extends 804 bp downstream of the insertion site.

(Wairkar et al., 2009, Toda et al., 2008)

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

Phenotype Manifest In

adult antennal lobe projection neuron | somatic clone

(Mochizuki et al., 2011)

adult CP2 lineage clone | somatic clone

(Mochizuki et al., 2011)

antennal lobe glomerulus | somatic clone

(Mochizuki et al., 2011)

antennal lobe glomerulus DA1 | somatic clone

(Mochizuki et al., 2011)

antennal lobe glomerulus DM2 | somatic clone

(Mochizuki et al., 2011)

antennal lobe glomerulus DM5 | somatic clone

(Mochizuki et al., 2011)

antennal lobe projection neuron | somatic clone

(Mochizuki et al., 2011)

axon & motor neuron | larval stage

(Wairkar et al., 2009)

calyx of larval mushroom body | somatic clone | third instar larval stage

(Mochizuki et al., 2011)

dendrite | adult stage | somatic clone

(Mochizuki et al., 2011)

dendrite | somatic clone | third instar larval stage

(Mochizuki et al., 2011)

embryonic/larval mushroom body | third instar larval stage

(Mochizuki et al., 2011)

neuromuscular junction (with Atg1²⁵)

(Wairkar et al., 2009)

neuromuscular junction | larval stage

(Wairkar et al., 2009)

neuromuscular junction | larval stage (with Atg1²⁵)

(Wairkar et al., 2009)

pedunculus of larval mushroom body | somatic clone | third instar larval stage

(Mochizuki et al., 2011)

presynaptic active zone & neuromuscular junction | larval stage

(Wairkar et al., 2009)

t-bar & neuromuscular junction | larval stage

(Wairkar et al., 2009)

Detailed Description

Statement

Reference

Atg1³ homozygous third instar larval mushroom bodies show prevalent disintegration of the core into multiple bundles and defects in the extension of calix dendrites, as compared to controls.

Atg1³ homozygous clones within mosaic third instar larval mushroom bodies show prevalent peduncle defects (split fascicles are observed in nearly half of cases) and defects in the extension of calix dendrites, although both the dorsal and the medial lobes do not show defects, as compared to control clones. The majority of Atg1³ homozygous lateral neuroblast clones lead to antennal lobe projection neurons fasciculation defects, although most of the anterodorsal neuroblast clones do not lead to obvious defects in axonal projections, as compared to control clones. Projection neurons clones show mild to severe ectopic innervation of the off-target glomeruli DA1, DM5 and DM2 glomeruli, but do not affect the VA2, VA1d, VA1lm, VA3, VM2, DM6, DL1 or VM7 glomeruli, as compared to controls.

Atg1³ homozygous DL1 clones lead to a small but significant increase in the number of branches in the calyx, but not in the number of terminal branches in the lateral horn, as compared to clones; a significant proportion of Atg1³ homozygous adult antennal lobe projection neuron clones (anterodorsal neuroblast clones, lateral neuroblast clones or ventral neuroblast clones) exhibit overextending dendrites, overshooting as compared to controls.

(Mochizuki et al., 2011)

Atg1³ heterozygous neuromuscular junctions exhibit wild-type bouton levels.

(Tian et al., 2011)

Marker analysis indicates that pre-and post synaptic component of the neuromuscular junction fail to align properly in Atg1³ homozygous or Atg1²⁵/Atg1³ heterozygous larvae. In addition, in Atg1³ homozygotes the size of neuromuscular junctions (NMJs) is reduced, as is the density of puncta within these junctions. This reduction in size appears not to be due to retraction of an initially normal sized NMJ, as there is not sign of junctional proteins on the muscle surface outside of the NMJ. Ultrastructural analysis reveals that, while many aspects ultrastructure of boutons in these mutants, they have lower densities of active zones, t-bars and active zones containing t-bars. These structural defects in NMJs are accompanied by an approximately 3 fold decrease in the amplitude of evoked excitatory junction potentials (EJPs). There is no accompanying change in spontaneous mini excitatory junction potential (mEJP) amplitude. Atg1³/Atg1^EY07351 NMJs show the same electrophysiological defects and also exhibit a significant decrease in mEJP frequency.

Accumulation of synaptic material is seen in the axons of motor neurons in Atg1³ homozygous larvae.

(Wairkar et al., 2009)

Atg1³/Atg1²⁵ and Atg1³/Df(3L)ED4486 animals show axonal transport defects at the larval stage.

(Toda et al., 2008)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Atg1³ has abnormal neurophysiology | recessive phenotype, suppressible by rl¹/rl¹

(Wairkar et al., 2009)

Suppressor of

Statement

Reference

Atg1³ is a suppressor | partially of visible phenotype of Scer\GAL4^bbg-C96, dom^RNAi.Sym.UAS

(Kwon et al., 2013)

Atg1³/Atg1³ is a suppressor of abnormal neurophysiology | recessive phenotype of rl¹

(Wairkar et al., 2009)

NOT Suppressor of

Statement

Reference

Atg1²⁵/Atg1³ is a non-suppressor of abnormal neuroanatomy | larval stage phenotype of fzy¹/fzy⁵⁰³²

(Kuang et al., 2014)

Atg1²⁵/Atg1³ is a non-suppressor of decreased cell number | larval stage phenotype of fzy¹/fzy⁵⁰³²

(Kuang et al., 2014)

Phenotype Manifest In

Suppressed by

Statement

Reference

Atg1³ has neuromuscular junction | larval stage phenotype, suppressible | partially by rl¹/rl¹

(Wairkar et al., 2009)

NOT suppressed by

Statement

Reference

Atg1³ has axon & motor neuron | larval stage phenotype, non-suppressible by rl¹/rl¹

(Wairkar et al., 2009)

Suppressor of

Statement

Reference

Atg1³ is a suppressor | partially of wing margin phenotype of Scer\GAL4^bbg-C96, dom^RNAi.Sym.UAS

(Kwon et al., 2013)

Atg1³/Atg1[+] is a suppressor of synapse phenotype of Rae1^EX28

(Tian et al., 2011)

Atg1³/Atg1[+] is a suppressor of NMJ bouton phenotype of Rae1^EX28

(Tian et al., 2011)

NOT Suppressor of

Statement

Reference

Atg1²⁵/Atg1³ is a non-suppressor of neuroblast | larval stage phenotype of fzy¹/fzy⁵⁰³²

(Kuang et al., 2014)

Additional Comments

Genetic Interactions

Statement

Reference

Atg1²⁵/Atg1³ does not suppress the neuroblast loss seen in fzy⁵⁰³²/fzy¹ mutant larval brains.

(Kuang et al., 2014)

The wing nicking phenotype caused by expression of dom^{dsRNA.Sym.Scer\UAS} under the control of Scer\GAL4^bbg-C96 is partially suppressed if the flies are also carrying Atg1³.

(Kwon et al., 2013)

An Atg1³ heterozygous background dominantly suppresses the increase in bouton number seen in Rae1^EX28 homozygous mutant neuromuscular junction.

(Tian et al., 2011)

The structural defects seen in the neuromuscular junctions (NMJ) of Atg1³ homozygous larvae are almost completely suppressed by rl¹/rl¹ : synaptic density and apposition of pre and post synaptic components are restored and NMJ size is partially restored. Despite the fact that evoked excitatory junction potentials at larval NMJs are decreased in both rl¹ homozygous and Atg1³ homozygous larvae, this phenotype is not see in rl¹ Atg1³ double homozygotes.