FlyBase Allele Report: Dmel\for[20-29]

General Information

Symbol

Dmel\for^20-29

Species

D. melanogaster

Name

FlyBase ID

FBal0319274

Feature type

allele

Associated gene

Dmel\for

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

Mutagen

CRISPR/Cas9

Nature of the Allele

Allele class

Mutagen

CRISPR/Cas9

(Peng et al., 2016)

Progenitor genotype

Cytology

Description

1bp deletion within the kinase domain that is conserved in all isoforms of for, resulting in a frame shift.

(Peng et al., 2016)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

deletion

2L:3,623,567..3,623,567 [-]

Comment:

1 bp deletion In coding sequence common to all isoforms causes a frameshift.

(Peng et al., 2016)

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 | dominant | embryonic stage

(Peng et al., 2016)

Phenotype Manifest In

axon | embryonic stage

(Peng et al., 2016)

larval intersegmental nerve branch ISNb of A1-7 | embryonic stage

(Peng et al., 2016)

Detailed Description

Statement

Reference

Motor axons of intersegmental nerve b (ISNb) in for^20-29/for^20-29 or for^20-29/+ mutant embryos display increases in targeting defects (overgrowth, targeting of incorrect muscles resulting in ectopic nerve endings, occasional abnormal associations with adjacent axons) compared to wild type.

(Peng et al., 2016)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

for^20-29 has abnormal neuroanatomy | dominant | embryonic stage phenotype, suppressible | partially by lola^T38-1/lola[+]

(Peng et al., 2016)

Suppressor of

Statement

Reference

for[+]/for^20-29 is a suppressor | partially of abnormal neuroanatomy | dominant | embryonic stage phenotype of lola^T38-1

(Peng et al., 2016)

Phenotype Manifest In

Suppressed by

Statement

Reference

for^20-29 has larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype, suppressible | partially by lola^T38-1/lola[+]

(Peng et al., 2016)

for^20-29 has axon | embryonic stage phenotype, suppressible | partially by lola^T38-1/lola[+]

(Peng et al., 2016)

Suppressor of

Statement

Reference

for[+]/for^20-29 is a suppressor | partially of larval intersegmental nerve branch ISNb of A1-7 | embryonic stage phenotype of lola^T38-1

(Peng et al., 2016)

for[+]/for^20-29 is a suppressor | partially of axon | embryonic stage phenotype of lola^T38-1

(Peng et al., 2016)

Additional Comments

Genetic Interactions

Statement

Reference

lola^T38-1/+;for^20-29/+ double heterozygous embryos show significant reduction of ISNb axon guidance defects compared to the single heterozygotes (lola^T38-1/+ or for^20-29/+).

(Peng et al., 2016)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Partially rescued by

for^20-29 is partially rescued by Scer\GAL4^elav.PU/for^UAS.cWb

(Peng et al., 2016)

Comments

Expression of for^Scer\UAS.cWb driven by Scer\GAL4^elav.PU partially rescues targeting defects of motor axons of intersegmental nerve b (ISNb) in for^20-29/for^20-29 embryos.

(Peng et al., 2016)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (1)

Reported As

Symbol Synonym

for^20-29

(Peng et al., 2016)

Name Synonyms

Secondary FlyBase IDs

References (1)

Report Sections

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