FlyBase Allele Report: Dmel\kra[2]

General Information

Symbol

Dmel\kra²

Species

D. melanogaster

Name

FlyBase ID

FBal0212936

Feature type

allele

Associated gene

Dmel\kra

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

Mutagen

P-element activity

Nature of the Allele

Allele class

Mutagen

P-element activity

(Lee et al., 2007)

Progenitor genotype

P{EP}kra^EP428

(Lee et al., 2007)

Cytology

Description

Imprecise excision of the P{EP} element, resulting in a 1404bp deletion of exba, corresponding to -1242 to +161 of the exba sequence.

(Lee et al., 2007)

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 neuroanatomy (with kra¹)

(Sanchez-Soriano et al., 2009)

abnormal neuroanatomy | embryonic stage (with kra¹)

(Lee et al., 2007)

Phenotype Manifest In

axon & pCC neuron (with kra¹)

(Lee et al., 2007)

filopodium (with kra¹)

(Sanchez-Soriano et al., 2009)

neuron (with kra¹)

(Sanchez-Soriano et al., 2009)

Detailed Description

Statement

Reference

exba¹/exba² primary neuronal cultures show normal microtubule organization but a significant reduction in filopodia number.

(Sanchez-Soriano et al., 2009)

In exba¹/exba² embryos, the pCC axon aberrantly crosses the midline in 18% of CNS segments.

(Lee et al., 2007)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

kra²/kra¹ has abnormal neuroanatomy | embryonic stage phenotype, enhanceable by shot³/shot[+]

(Lee et al., 2007)

Enhancer of

Statement

Reference

exba[+]/kra² is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of sli²

(Lee et al., 2007)

exba[+]/kra² is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of shot³/shot[+], sli²

(Lee et al., 2007)

exba[+]/kra² is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of shot³

(Lee et al., 2007)

kra²/kra¹ is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of shot³

(Lee et al., 2007)

exba[+]/kra² is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of robo1²

(Lee et al., 2007)

exba[+]/kra² is an enhancer of abnormal neuroanatomy | embryonic stage phenotype of robo1², shot³

(Lee et al., 2007)

Other

Statement

Reference

kra², shot^SF20/shot[+] has abnormal neuroanatomy phenotype

(Sanchez-Soriano et al., 2009)

Phenotype Manifest In

Enhanced by

Statement

Reference

kra²/kra¹ has axon & pCC neuron phenotype, enhanceable by shot³/shot[+]

(Lee et al., 2007)

Enhancer of

Statement

Reference

exba[+]/kra² is an enhancer of axon & pCC neuron phenotype of sli²

(Lee et al., 2007)

exba[+]/kra² is an enhancer of axon & pCC neuron phenotype of shot³/shot[+], sli²

(Lee et al., 2007)

exba[+]/kra² is an enhancer of axon & pCC neuron phenotype of shot³

(Lee et al., 2007)

kra²/kra¹ is an enhancer of axon & pCC neuron phenotype of shot³

(Lee et al., 2007)

exba[+]/kra² is an enhancer of axon & pCC neuron phenotype of robo1²

(Lee et al., 2007)

exba[+]/kra² is an enhancer of axon & pCC neuron phenotype of robo1², shot³

(Lee et al., 2007)

Other

Statement

Reference

kra², shot^SF20/shot[+] has neuron phenotype

(Sanchez-Soriano et al., 2009)

kra², shot^SF20/shot[+] has filopodium phenotype

(Sanchez-Soriano et al., 2009)

Additional Comments

Genetic Interactions

Statement

Reference

shot^SF20/+ exba²/+ primary neuronal cultures show a strong reduction in filopodia number, whereas controls heterozygous for only one of these genes display normal filopodia.

(Sanchez-Soriano et al., 2009)

The axon midline phenotype of sli²/+ embryos is enhanced in sli²/+; exba²/+ and shot³/+, sli²/+ double mutants. The phenotype is further enhanced in shot³/+, sli²/+; exba²/+ triple mutants.

(Lee et al., 2007)

The frequency of aberrant pCC axon midline crossovers in shot³/+; exba¹/exba² and shot³/shot³; exba²/+ double mutant embryos is significantly greater than in either single mutant homozygous embryos. The midline crossing phenotype is slightly more severe in shot³/shot³; exba¹/exba² embryos compared to shot³/shot³; exba²/+ embryos, while shot³/+; exba²/+ embryos show no significant midline defects.

The pCC axon midline crossing phenotype of robo² embryos is dramatically enhanced in robo²/+; exba²/+ embryos and in shot³, robo²/+ embryos. The phenotype is further enhanced in shot³, robo²/+; exba²/+ embryos.