FlyBase Allele Report: Dmel\kuz[unspecified]

General Information

Symbol

Dmel\kuz^unspecified

Species

D. melanogaster

Name

FlyBase ID

FBal0057209

Feature type

allele

Associated gene

Dmel\kuz

Associated Insertion(s)

Carried in Construct

Key Links

Allele class

Mutagen

Nature of the Allele

Allele class

Mutagen

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

abnormal neuroanatomy | embryonic stage 16

(Coleman et al., 2010)

Phenotype Manifest In

commissure | embryonic stage 16

(Coleman et al., 2010)

larval longitudinal connective

(Schimmelpfeng et al., 2001, Fambrough et al., 1996)

larval longitudinal connective | embryonic stage 16

(Coleman et al., 2010)

larval ventral nerve cord commissure

(Schimmelpfeng et al., 2001)

symmetrical commissure

(Fambrough et al., 1996)

Detailed Description

Statement

Reference

kuz^unspecified stage 16 embryos exhibit thinning of the longitudinals and thickening of the commissures as well as mild ectopic ap neuron crossing. Ipsilateral axons from the medial and intermediate fascicles aberrantly cross the midline. Kuz[unspecified] embryos do not display any cell fate defects.

(Coleman et al., 2010)

Heart beating is observed in homozygous kuz mutant embryos, although beating is irregular, probably due to the misarrangement of cardioblasts.

(Albrecht et al., 2006)

Mutant embryos show a partial fusion of segmental commissures. The longitudinal connectives are reduced in size. Many Fas2-positive axons cross the midline. Mutant embryos do not have head defects.

(Schimmelpfeng et al., 2001)

Embryos that are null for kuz gene product (derived from germ line clones) show no processed form of the Dl gene product.

(Qi et al., 1999)

Embryos show a reduction in the thickness of the longitudinal connectives of the central nervous system (CNS), accompanied by an accumulation of axonal material in the commissural region. This is due to a failure of longitudinal axon bundles to extend through the intercommissural region. The pCC neuron extends its axon normally through the intercommissural region, and the aCC motoneuron extends its axon a large distance out of the CNS, as seen in wild-type embryos.

(Fambrough et al., 1996)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

kuz^unspecified has abnormal neuroanatomy | embryonic stage 16 phenotype, enhanceable by sli^unspecified/robo1^unspecified

(Coleman et al., 2010)

NOT Enhancer of

Statement

Reference

kuz^unspecified is a non-enhancer of abnormal neuroanatomy | embryonic stage 16 phenotype of robo1^unspecified

(Coleman et al., 2010)

Suppressor of

Statement

Reference

kuz^unspecified is a suppressor of abnormal neuroanatomy | embryonic stage 16 phenotype of comm^Δe39

(Coleman et al., 2010)

Phenotype Manifest In

Enhanced by

Statement

Reference

kuz^unspecified has larval longitudinal connective | embryonic stage 16 phenotype, enhanceable by sli^unspecified/robo1^unspecified

(Coleman et al., 2010)

kuz^unspecified has commissure | embryonic stage 16 phenotype, enhanceable by sli^unspecified/robo1^unspecified

(Coleman et al., 2010)

NOT Enhancer of

Statement

Reference

kuz^unspecified is a non-enhancer of larval longitudinal connective | embryonic stage 16 phenotype of robo1^unspecified

(Coleman et al., 2010)

kuz^unspecified is a non-enhancer of commissure | embryonic stage 16 phenotype of robo1^unspecified

(Coleman et al., 2010)

kuz[+]/kuz^unspecified is a non-enhancer of phenotype of sli^unspecified

(Schimmelpfeng et al., 2001)

Suppressor of

Statement

Reference

kuz^unspecified is a suppressor of larval longitudinal connective | embryonic stage 16 phenotype of comm^Δe39

(Coleman et al., 2010)

kuz^unspecified is a suppressor of commissure | embryonic stage 16 phenotype of comm^Δe39

(Coleman et al., 2010)

Other

Statement

Reference

kuz^unspecified, sli^unspecified/sli[+] has presumptive embryonic/larval central nervous system phenotype

(Schimmelpfeng et al., 2001)

kuz^unspecified, sli^unspecified has presumptive embryonic/larval central nervous system phenotype

(Schimmelpfeng et al., 2001)

Additional Comments

Genetic Interactions

Statement

Reference

kuz^unspecified does not enhance the FasII axon midline crossing phenotype seen in robo^unspecified stage 16 embryos.

kuz^unspecified partially suppresses the loss of commissures seen in comm^Δe39 homozygous stage 16 embryos, although most axons are still unable to cross the midline.

(Coleman et al., 2010)

Fas2-positive axons cross the central nervous system midline in about 12% of sli^unspecified kuz^unspecified double heterozygotes, in contrast to either single heterozygote. kuz^unspecified homozygotes that are also heterozygous for sli^unspecified have a central nervous system (CNS) phenotype similar to kuz^unspecified single mutants, but the position of the longitudinal connectives is shifted towards the CNS midline. Removal of one copy of kuz⁺ in a sli^unspecified homozygous background does not enhance the sli mutant phenotype. robo^unspecified homozygotes that are also heterozygous for kuz^unspecified have a central nervous system (CNS) phenotype similar to that of robo^unspecified single mutants. The overall axon phenotype of robo^unspecified kuz^unspecified double homozygotes is slightly more severe than that of robo^unspecified single mutants as axons are frequently detected running along the CNS midline.

(Schimmelpfeng et al., 2001)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

kuz^unspecified is rescued by kuz^UAS.Tag:HA/Scer\GAL4^elav.PLu

(Coleman et al., 2010)

kuz^unspecified is rescued by kuz^UAS.cCa/Scer\GAL4^elav.PLu

(Coleman et al., 2010)

kuz^unspecified is rescued by Scer\GAL4^elav-C155/kuz^UAS.cFa

(Fambrough et al., 1996)

Not rescued by

kuz^unspecified is not rescued by kuz^UAS.Tag:HA/Scer\GAL4^sli.PS

(Coleman et al., 2010)

kuz^unspecified is not rescued by kuz^UAS.cCa/Scer\GAL4^sli.PS

(Coleman et al., 2010)

Comments

Expression of kuz^Scer\UAS.cCa in all post-mitotic neurons using Scer\GAL4^elav.PLu fully rescues the midline crossing phenotype seen in kuz^unspecified stage 16 embryos.

Expression of kuz^{Scer\UAS.T:Ivir\HA1} in all post mitotic neurons using Scer\GAL4^elav.PLu fully rescues the midline crossing phenotype seen in kuz^unspecified stage 16 embryos.

Expression of kuz^Scer\UAS.cCa in midline glia using Scer\GAL4^sli.PS fails to rescue the midline crossing phenotype seen in kuz^unspecified stage 16 embryos.

Expression of kuz^{Scer\UAS.T:Ivir\HA1} in midline glia using Scer\GAL4^sli.PS fails to rescue the midline crossing phenotype seen in kuz^unspecified stage 16 embryos.

(Coleman et al., 2010)

The defect in axon tract formation is rescued by kuz^Scer\UAS.cFa expression driven by Scer\GAL4^elav-C155.

(Fambrough et al., 1996)

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

kuz^unspecified

unspecified

(Fambrough et al., 1996)

Name Synonyms

Secondary FlyBase IDs

References (6)

Report Sections

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