FlyBase Allele Report: Dmel\cv-c[1]

General Information

Symbol

Dmel\cv-c¹

Species

D. melanogaster

Name

FlyBase ID

FBal0002188

Feature type

allele

Associated gene

Dmel\cv-c

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

Mutagen

spontaneous

Nature of the Allele

Allele class

Mutagen

spontaneous

Progenitor genotype

Cytology

Description

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

Phenotype Manifest In

Detailed Description

Statement

Reference

cv-c¹ heterozygous or homozygous adults exhibit wings with partially missing posterior crossvein compared to controls.

(Jantrapirom et al., 2019)

cv-c¹ mutant pupal wings lack the presumptive posterior crossvein but the organization of the extracellular matrix appears unperturbed.

(Schleede and Blair, 2015)

Most of the posterior crossvein is missing in homozygous cv-c¹ mutants. The remnant of the posterior crossvein is detached, it does not reach the fourth and fifth longitudinal wing veins.

The posterior crossvein appears normal in cv-c¹ heterozygotes.

Miniature excitatory junction potentials (mEJPs) recorded at third instar larval neuromuscular junctions of homozygous cv-c¹ mutants are not significantly different from that of wild-type larvae.

The amplitudes of excitatory junction potentials (EJPs) evoked by stimulation at 0.3 Hz and recorded at third instar larval neuromuscular junctions of homozygous cv-c¹ and heterozygous cv-c¹/+ or trans-heterozygous cv-c¹/cv-c^C524 and cv-c¹/cv-c^M62 mutants are significantly increased above control levels. As a result, quantal content (QC) is about 70% higher than the QC in the wild-type control.

Expression of cv-c^Scer\UAS.cDa in motoneurons under the control of Scer\GAL4^OK6 fails to rescue the abnormal quantal content (QC) phenotype of cv-c¹/+ larvae.

Expression of cv-c^Scer\UAS.cDa in muscle under the control of Scer\GAL4^G14 rescues the abnormal quantal content (QC) phenotype of cv-c¹/+ larvae.

There is an increase in the number of T-bars at cv-c¹ mutant neuromuscular junctions relative to controls.

(Pilgram et al., 2011)

In the wings of cv-c¹ flies the posterior crossvein is completely absent and the anterior crossvein is detached from the fourth longitudinal vein. cv-c¹/cv-c^M62 wings display the same posterior crossvein phenotype.

(Denholm et al., 2005)

Posterior crossvein usually absent or greatly reduced. Anterior crossvein usually present but often detached. Eye flattened or with vertical shallow furrow. Legs weak, especially tarsal joints. Occasionally overlaps wild type. RK2.

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

cv-c¹ has visible | adult stage phenotype, enhanceable by Dyb¹¹

(Jantrapirom et al., 2019)

Suppressed by

Statement

Reference

cv-c¹ has abnormal neurophysiology | dominant phenotype, suppressible | partially by Scer\GAL4^G14/Dys^GS12472

(Pilgram et al., 2011)

Other

Statement

Reference

Dys^E6, cv-c¹ has visible | dominant phenotype

(Pilgram et al., 2011)

Phenotype Manifest In

Enhanced by

Statement

Reference

cv-c¹ has posterior crossvein phenotype, enhanceable by Dyb¹¹

(Jantrapirom et al., 2019)

cv-c¹ has wing phenotype, enhanceable by Dyb¹¹

(Jantrapirom et al., 2019)

Suppressed by

Statement

Reference

cv-c¹ has neuromuscular junction phenotype, suppressible | partially by Scer\GAL4^G14/Dys^GS12472

(Pilgram et al., 2011)

Additional Comments

Genetic Interactions

Statement

Reference

Dyb¹¹ heterozygosity or homozygosity enhances the posterior crossvein phenotype of cv-c¹ heterozygous adults.

(Jantrapirom et al., 2019)

Most of the posterior crossvein is missing in Dys^E6/+, cv-c¹/+ double heterozygotes. The remnant of the posterior crossvein is detached, it does not reach the fourth and fifth longitudinal wing veins.

The increased quantal content (QC) measured at the neuromuscular junction of cv-c¹/+ mutants is reduced as a result of expression of Dys^GS12472 under the control of Scer\GAL4^G14.

Heterozygosity for Cdc42⁴ in a cv-c¹/+ mutant background restores quantal content (QC) to wild-type levels.

(Pilgram et al., 2011)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

cv-c¹ is rescued by Scer\GAL4^G14/cv-c^UAS.cDa

(Pilgram et al., 2011)

Not rescued by

cv-c¹ is not rescued by Scer\GAL4^RapGAP1-OK6/cv-c^UAS.cDa

(Pilgram et al., 2011)

Comments

Expression of cv-c^Scer\UAS.cDa in motoneurons under the control of Scer\GAL4^OK6 fails to rescue the abnormal quantal content (QC) phenotype of cv-c¹/+ larvae.

Expression of cv-c^Scer\UAS.cDa in muscle under the control of Scer\GAL4^G14 rescues the abnormal quantal content (QC) phenotype of cv-c¹/+ larvae.

(Pilgram et al., 2011)

Images (1)

Holtzman, S. and Kaufman, T. (2013)

Mutant

Wild-type