FlyBase Allele Report: Dmel\Cln3[ΔMB1]

General Information

Symbol

Dmel\Cln3^ΔMB1

Species

D. melanogaster

Name

FlyBase ID

FBal0263822

Feature type

allele

Associated gene

Dmel\Cln3

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

amorphic allele - molecular evidence

Mutagen

transposable element activity

Nature of the Allele

Allele class

amorphic allele - molecular evidence

(Tuxworth et al., 2011)

Mutagen

transposable element activity

(Tuxworth et al., 2011)

Progenitor genotype

Mi{ET1}Cln3^MB06009

(Tuxworth et al., 2011)

Cytology

Description

Imprecise excision of Mi{ET1}cln3^MB06009 deleting 1534 bp including the predicted translation start site and the first 102 codons of cln3.

(Tuxworth et al., 2011)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

3L:17,810,612..17,811,956 [-]

Comment:

1534 bp deletion resulting from the imprecise excision of Mi{ET1}Cln3^MB06009, which removes the first 102 codons of Cln3

(Tuxworth et al., 2011)

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 neuronal ceroid lipofuscinosis 1

CEA

(Wong et al., 2015)

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 | third instar larval stage

(Wong et al., 2015)

abnormal oxidative stress response | recessive

(Tuxworth et al., 2011)

abnormal starvation stress response | female limited | recessive

(Tuxworth et al., 2011)

fertile

(Tuxworth et al., 2011)

short lived | recessive

(Tuxworth et al., 2011)

viable

(Tuxworth et al., 2011)

Phenotype Manifest In

embryonic/larval neuromuscular junction | third instar larval stage

(Wong et al., 2015)

NMJ bouton | third instar larval stage

(Wong et al., 2015)

Detailed Description

Statement

Reference

The number of neuromuscular junction boutons is significantly lower in cln3^ΔMB1 homozygous larvae than in the cln3^ΔMB1/+ controls.

(Wong et al., 2015)

Homozygous cln3^ΔMB1 mutant flies are viable and fertile with no obvious developmental abnormalities. The viability of cln3^ΔMB1 mutant embryos is reduced by a small degree, but survival of first instar and larvae to adulthood is unaffected.

Homozygous cln3^ΔMB1 mutant flies are hypersensitive to oxidative stress and display reduced lifespan when compared with control animals. Homozygous cln3^ΔMB1 mutant flies are unable to detoxify the reactive oxygen species that accumulate when exposed to conditions of oxidative stress.

The thermal stress response of homozygous cln3^ΔMB1 flies (as measured by the time for recovery from cold-induced coma and survival times at 37[o]C) does not differ from that of wild-type controls.

Homozygous cln3^ΔMB1 mutants do not show more sensitivity to increasing osmotic stress during development than do wild-type controls.

Homozygous cln3^ΔMB1 mutant females show significantly more resistance to starvation than wild-type flies. Males show no difference.

(Tuxworth et al., 2011)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

Cln3^ΔMB1 has abnormal neuroanatomy | third instar larval stage phenotype, suppressible by Scer\GAL4^elav-C155/RagA-B^Q61L.UAS

(Wong et al., 2015)

Other

Statement

Reference

cln3[+]/Cln3^ΔMB1, Trpml¹ has abnormal neuroanatomy | third instar larval stage phenotype

(Wong et al., 2015)

Phenotype Manifest In

Suppressed by

Statement

Reference

Cln3^ΔMB1 has embryonic/larval neuromuscular junction | third instar larval stage phenotype, suppressible by Scer\GAL4^elav-C155/RagA-B^Q61L.UAS

(Wong et al., 2015)

Cln3^ΔMB1 has NMJ bouton | third instar larval stage phenotype, suppressible by Scer\GAL4^elav-C155/RagA-B^Q61L.UAS

(Wong et al., 2015)

Other

Statement

Reference

cln3[+]/Cln3^ΔMB1, Trpml¹ has neuromuscular junction | third instar larval stage phenotype

(Wong et al., 2015)

cln3[+]/Cln3^ΔMB1, Trpml¹ has NMJ bouton | third instar larval stage phenotype

(Wong et al., 2015)

Additional Comments

Genetic Interactions

Statement

Reference

Trpml¹/+,cln3^ΔMB1/+ double heterozygotes show decreased number of NMJ boutons in third instar larvae compared to either Trpml¹/+ or cln3^ΔMB1/+ single heterozygotes.

Ectopic expression of RagA-B^{Q61L.Scer\UAS} under the control of the Scer\GAL4^elav-C155 driver fully restores the decreased number of neuromuscular junction boutons characteristic for the cln3^ΔMB1 mutant third instar larvae.

(Wong et al., 2015)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Cln3^ΔMB1 is rescued by Cln3^UAS.Venus

(Tuxworth et al., 2011)

Comments

Ubiquitous expression of cln3^{Scer\UAS.T:Avic\GFP-YFP.Venus} under the control of Scer\GAL4^arm.PS rescues the hypersensitivity of cln3^ΔMB1 mutants to oxidative stress. The shortened lifespan of cln3^ΔMB1 homozygotes is also rescued by the expression of cln3^{Scer\UAS.T:Avic\GFP-YFP.Venus} via Scer\GAL4^arm.PS.

(Tuxworth et al., 2011)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (2)

Reported As

Symbol Synonym

Cln3^ΔMB1

cln3^ΔMB1

(Wong et al., 2015, Tuxworth et al., 2011)

Name Synonyms

Secondary FlyBase IDs

References (2)

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