FlyBase Allele Report: Dmel\Dys[Dp186.166.3]

General Information

Symbol

Dmel\Dys^Dp186.166.3

Species

D. melanogaster

Name

FlyBase ID

FBal0246198

Feature type

allele

Associated gene

Dmel\Dys

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Fradkin et al., 2008)

Progenitor genotype

Dys^GE20705

(Fradkin et al., 2008)

Cytology

Description

Imprecise excision of P{EP}Dys^GE20705 generates a 1.2kb deletion removing the Dp186 ATG codon and most of the unique first exon of Dp186.

(Fradkin et al., 2008)

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 chemosensory behavior | adult stage

(Jantrapirom et al., 2019)

abnormal locomotor behavior | adult stage

(Jantrapirom et al., 2019)

abnormal neurophysiology

(Fradkin et al., 2008)

Phenotype Manifest In

Detailed Description

Statement

Reference

Dys^Dp186.166.3 mutant adults have significantly reduced benzaldehyde avoidance, compared to controls; there is no effect on axon guidance, innervation pattern or dendritic morphology of olfactory receptor neurons, compared to controls.

(Jantrapirom et al., 2019)

Voltage-clamp recordings from either the aCC or RP2 motor neurons reveals that synaptic currents are significantly increased in amplitude in Dys^Dp186.166.3 homozygous and heterozygous mutants. Cumulative probability plots of individual synaptic currents reveals that there is a significant increase in amplitudes of the majority of the individual currents measured, compared with wild-type controls.

The frequency of action potential-dependent synaptic currents recorded in aCC/RP2 is not significantly altered in Dys^Dp186.166.3 mutants compared to wild-type.

The presence of TTX has no effect on the ampltiude of miniature synaptic currents (mEPSCs) in aCC/RP2 neurons in Dys^Dp186.166.3 mutants. The frequency is, however, significantly increased compared to controls, indicating a heightened probability of presynaptic vesicle release.

(Fradkin et al., 2008)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

NOT Enhanced by

Statement

Reference

Dys^Dp186.166.3 has abnormal neurophysiology phenotype, non-enhanceable by gbb¹/gbb[+]

(Fradkin et al., 2008)

NOT suppressed by

Statement

Reference

Dys^Dp186.166.3 has abnormal neurophysiology phenotype, non-suppressible by gbb¹/gbb[+]

(Fradkin et al., 2008)

Suppressor of

Statement

Reference

Dys^Dp186.166.3 is a suppressor of abnormal neurophysiology phenotype of gbb¹

(Fradkin et al., 2008)

Phenotype Manifest In

Additional Comments

Genetic Interactions

Statement

Reference

In a gbb¹ heterozygous mutant, with only one copy of wild-type gbb, the absence of Dp186 through a Dys^Dp186.166.3 homozygous background is sufficient to increase synaptic currents to a level comparable to that observed in Dys^Dp186.166.3 mutants with wild-type levels of gbb expression.

Double homozygous gbb¹; Dys^Dp186.166.3 mutants display increased synaptic currents relative to gbb¹ mutants.

(Fradkin et al., 2008)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

Dys^Dp186.166.3 is rescued by Dys^Dp186.UAS/Scer\GAL4^GH146

(Jantrapirom et al., 2019)

Dys^Dp186.166.3 is rescued by Dys^Dp186.UAS/Scer\GAL4^SG18.1

(Jantrapirom et al., 2019)

Dys^Dp186.166.3 is rescued by Scer\GAL4^elav.PU/Dys^Dp186.UAS