FlyBase Allele Report: Dmel\atl[RNAi.UAS]

General Information

Symbol

Dmel\atl^RNAi.UAS

Species

D. melanogaster

Name

FlyBase ID

FBal0244003

Feature type

allele

Associated gene

Dmel\atl

Associated Insertion(s)

Carried in Construct

P{UAS-atl-RNAi}

Also Known As

UAS-atl^RNAi, atlRNAi

Key Links

Transgenic product class

RNAi_reagent

(Orso et al., 2009)

Mutagen

in vitro construct

Nature of the Allele

Transgenic product class

RNAi_reagent

(Orso et al., 2009)

Mutagen

in vitro construct

(Orso et al., 2009)

Progenitor genotype

Carried in construct

P{UAS-atl-RNAi}

Cytology

Description

UAS regulatory sequences drive expression of an inverted repeat of a fragment of a atl cDNA.

(Orso et al., 2009)

Allele components

Component

Use(s)

Regulatory region(s)

UAS

binary expression system - regulatory region

Encoded product / tool

atl

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 hereditary spastic paraplegia

CEA

(Summerville et al., 2016)

model of hereditary spastic paraplegia 3A

CEA

(Srivastav et al., 2024, Srivastav et al., 2024, Xu et al., 2017)

Modifiers Based on Experimental Evidence ( 1 )

Disease

Interaction

References

model of hereditary spastic paraplegia 3A

is ameliorated by mTor^k17004

(Xu et al., 2017)

is exacerbated by TrpA1^{13xlexAop.JFRC26}

(Srivastav et al., 2024)

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

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

Phenotype Manifest In

Detailed Description

Statement

Reference

Expression of atl^{dsRNA.Scer\UAS} driven by Scer\GAL4^nSyb.PS decreases endoplasmic reticulum (ER) tubule crossbridges (and ER tubules become wavy) in motor neuron axon initial segments and a diffuse ER fragmentation at motor nerve terminals of third instar larvae.

Expression of atl^{dsRNA.Scer\UAS} driven by Scer\GAL4^elav-C155 (along with UAS-dcr) does not significantly affect quantal content or mini EJP amplitude (1.5 mM Ca[2+]) at the neuromuscular junction of third instar larvae compared to controls.

Expression of atl^{dsRNA.Scer\UAS} (along with UAS-dcr) driven by Scer\GAL4^Toll-6-D42 or Scer\GAL4^elav-C155 (at 0.1 mM Ca[2+]) significantly reduces EJP amplitude at the third instar larval NMJ; reduction in EJP corresponds with a decrease in the frequency of successful synaptic transmission. Expression driven by Scer\GAL4^Mef2.PR or Scer\GAL4^Gli.PU does not significantly affect EJP amplitude or synaptic failure rate.

Expression of atl^{dsRNA.Scer\UAS} (along with UAS-dcr) driven by Scer\GAL4^elav-C155 significantly increases neuromuscular junction bouton number and leads to significant age-dependent locomotor deficits (significant decreases in time required to climb 6cm and walking velocity) in adult flies.

(Summerville et al., 2016)

Ultrastructural analysis shows considerable alterations in endoplasmic reticulum (ER) morphology in neurons and muscles as a result of atl^{dsRNA.Scer\UAS} expression driven by Scer\GAL4^αTub84B.PL. Control neurons have long tubular ER profiles, whereas neurons expressing atl^{dsRNA.Scer\UAS} show severely undersized ER profiles.

Repetitive photobleaching experiments suggest that the ER network is fragmented in muscle cells as a result of atl^{dsRNA.Scer\UAS} expression driven by Scer\GAL4^αTub84B.PL.

(Orso et al., 2009)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Scer\GAL4^elav-C155, atl^RNAi.UAS has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Rtnl1^GD900, Scer\GAL4^elav-C155

(Summerville et al., 2016)

Suppressor of

Statement

Reference

atl^RNAi.UAS, Scer\GAL4^elav-C155 is a suppressor of abnormal neuroanatomy | third instar larval stage phenotype of Rtnl1^GD900, Scer\GAL4^elav-C155

(Summerville et al., 2016)

Phenotype Manifest In

Suppressed by

Statement

Reference

Scer\GAL4^elav-C155, atl^RNAi.UAS has NMJ bouton | third instar larval stage phenotype, suppressible by Rtnl1^GD900, Scer\GAL4^elav-C155

(Summerville et al., 2016)

Suppressor of

Statement

Reference

atl^RNAi.UAS, Scer\GAL4^elav-C155 is a suppressor of NMJ bouton | third instar larval stage phenotype of Rtnl1^GD900, Scer\GAL4^elav-C155

(Summerville et al., 2016)

Additional Comments

Genetic Interactions

Statement

Reference

Co-expression of Rtnl1^GD900 significantly suppresses the increases in neuromuscular junction bouton number seen in Scer\GAL4^elav-C155>atl^{dsRNA.Scer\UAS} third instar larvae (and vice versa).

(Summerville et al., 2016)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Comments

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

604908

w^*; P{UAS-atl-RNAi}2, P{UAS-Dcr-2.D}2

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

atl^RNAi.UAS

atl^{dsRNA.Scer\UAS}

atl^dsRNA.UAS

Name Synonyms

Secondary FlyBase IDs

References (7)

Report Sections

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