FlyBase Allele Report: Dmel\unc-5[8]

General Information

Symbol

Dmel\unc-5⁸

Species

D. melanogaster

Name

FlyBase ID

FBal0193802

Feature type

allele

Associated gene

Dmel\unc-5

Associated Insertion(s)

Carried in Construct

Also Known As

unc5⁸

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

loss of function allele

(Labrador, 2005)

Mutagen

ethyl methanesulfonate

(Labrador, 2005)

Progenitor genotype

Cytology

Description

Amino acid replacement: Q19term.

(Labrador, 2005)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2R:15,357,082..15,357,082 [+]

Nucleotide change:

C15357082T

Amino acid change:

Q19term | unc-5-PA; Q19term | unc-5-PB

Reported amino acid change:

Q19term

Comment:

Site of nucleotide substitution in mutant inferred by FlyBase based on reported amino acid change.

(Labrador, 2005)

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 ( 1 )

Disease

Interaction

References

ameliorates amyotrophic lateral sclerosis type 15

modeled by Hsap\UBQLN2^P4X.UAS

(Kim et al., 2023)

Comments on Models/Modifiers Based on Experimental Evidence ( 0 )

Disease-implicated variant(s)

Phenotypic Data

Phenotypic Class

abnormal cell migration | dominant | embryonic stage

(Raza and Jacobs, 2016)

abnormal neuroanatomy

(Zarin et al., 2014, Labrador, 2005)

abnormal neuroanatomy (with Df(2R)XTE-18)

(Labrador, 2005)

abnormal neuroanatomy (with unc-5²)

(Labrador, 2005)

abnormal neuroanatomy | embryonic stage

(von Hilchen et al., 2010)

Phenotype Manifest In

Detailed Description

Statement

Reference

unc-5⁸ homozygous embryonic heart cardioblasts show significant decreases in migration velocity, as well as in filopodial and lamellopodial extensions and activities, as compared to controls; these are associated with gaps in the leading edge, cell clumping, improper linear alignment of the cardioblasts, and embryonic heart lumen formation defects, as compared to controls. unc-5⁸ heterozygous cardioblasts also show a significant decrease in migration velocity and filopodial activity, but not in lamellopodial activity, as compared to controls.

(Raza and Jacobs, 2016)

unc-5⁸ single mutants exhibit mild defects in motoneuron intersegmental nerve axon guidance.

(Zarin et al., 2014)

The number of embryonic peripheral glia (ePG) present on the intersegmental nerve distal to the SNc nerve branch is reduced compared to wild type. Positional and marker expression analysis indicates that it is the ePG6 and ePG8 cells which are missing from the intersegmental nerve distal to the SNc nerve branch, and they are instead either stalled in the exit area proximal to the SNc or fail to leave the central nervous system. ePG5 also occasionally stalls in the exit area.

(von Hilchen et al., 2010)

28% of unc-5⁸ mutants show a SNa guidance phenotype; 22% of unc-5⁸/Df(2R)XTE-18 and 19% of unc-5⁸/unc-5² transheterozygotes also show this phenotype.

(Labrador, 2005)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

unc-5⁸ has abnormal neuroanatomy phenotype, enhanceable by beat-Ia^C163/Nrg^l10/beat-Ia³

(Zarin et al., 2014)

unc-5⁸ has abnormal neuroanatomy phenotype, enhanceable by beat-Ia^C163/beat-Ia³

(Zarin et al., 2014)

unc-5⁸ has abnormal neuroanatomy phenotype, enhanceable by eve^ΔRP2A/beat-Ia[+]/eve[+]/beat-Ia³

(Zarin et al., 2014)

unc-5⁸ has abnormal neuroanatomy phenotype, enhanceable by eve^ΔRP2A/eve[+]

(Zarin et al., 2014)

unc-5⁸ has abnormal neuroanatomy phenotype, enhanceable by Nrg^l10

(Zarin et al., 2014)

NOT Enhanced by

Statement

Reference

beat-Ia^C163/beat-Ia³, unc-5⁸ has abnormal neuroanatomy phenotype, non-enhanceable by Nrg^l10

(Zarin et al., 2014)

Suppressed by

Statement

Reference

unc-5⁸ has abnormal cell migration | dominant | embryonic stage phenotype, suppressible | partially by robo1¹/robo1[+]

(Raza and Jacobs, 2016)

NOT suppressed by

Statement

Reference

beat-Ia^C163/beat-Ia³, unc-5⁸ has abnormal neuroanatomy phenotype, non-suppressible by Nrg^l10

(Zarin et al., 2014)

Enhancer of

Statement

Reference

unc-5[+], beat-Ia[+], unc-5⁸, beat-Ia³ is an enhancer of abnormal neuroanatomy phenotype of eve^ΔRP2A

(Zarin et al., 2014)

unc-5[+]/unc-5⁸ is an enhancer of abnormal neuroanatomy phenotype of eve^ΔRP2A

(Zarin et al., 2014)

unc-5[+]/unc-5⁸ is an enhancer of abnormal neuroanatomy phenotype of eve³

(Zarin et al., 2014)

unc-5[+], beat-Ia^C163, beat-Ia[+], unc-5⁸ is an enhancer of abnormal neuroanatomy phenotype of eve³

(Zarin et al., 2014)

Suppressor of

Statement

Reference

unc-5⁸ is a suppressor of abnormal eye color phenotype of Hsap\UBQLN2^P4X.UAS, Scer\GAL4^GMR.PU

(Kim et al., 2023)

unc-5[+]/unc-5⁸ is a suppressor of abnormal cell migration | dominant | embryonic stage phenotype of robo1¹

(Raza and Jacobs, 2016)

unc-5⁸ is a suppressor | partially of abnormal neuroanatomy phenotype of Scer\GAL4^eg-Mz360, eve^UAS.cBa

(Zarin et al., 2014)

beat-Ia^C163, unc-5⁸, beat-Ia³ is a suppressor | partially of abnormal neuroanatomy phenotype of Scer\GAL4^eg-Mz360, eve^UAS.cBa

(Zarin et al., 2014)

Other

Statement

Reference

grn^7L, unc-5[+]/unc-5⁸ has abnormal neuroanatomy | embryonic stage phenotype

(Zarin et al., 2012)

Df(2R)eve, eve^ΔRP2A, unc-5⁸ has abnormal neuroanatomy phenotype

(Zarin et al., 2012)

Phenotype Manifest In

Enhanced by

Statement

Reference

unc-5⁸ has embryonic heart cardioblast phenotype, enhanceable by robo1¹/robo1[+]

(Raza and Jacobs, 2016)

unc-5⁸ has filopodium | embryonic stage phenotype, enhanceable by robo1¹/robo1[+]

(Raza and Jacobs, 2016)

unc-5⁸ has larval intersegmental nerve phenotype, enhanceable by beat-Ia^C163/Nrg^l10/beat-Ia³

(Zarin et al., 2014)

unc-5⁸ has motor neuron phenotype, enhanceable by beat-Ia^C163/beat-Ia³

(Zarin et al., 2014)

unc-5⁸ has larval intersegmental nerve phenotype, enhanceable by eve^ΔRP2A/beat-Ia[+]/eve[+]/beat-Ia³

(Zarin et al., 2014)

unc-5⁸ has larval intersegmental nerve phenotype, enhanceable by eve^ΔRP2A/eve[+]

(Zarin et al., 2014)

unc-5⁸ has motor neuron phenotype, enhanceable by Nrg^l10

(Zarin et al., 2014)

unc-5⁸ has larval intersegmental nerve phenotype, enhanceable by Nrg^l10

(Zarin et al., 2014)

NOT Enhanced by

Statement

Reference

unc-5⁸ has lamellipodium | embryonic stage phenotype, non-enhanceable by robo1¹/robo1[+]

(Raza and Jacobs, 2016)

beat-Ia^C163/beat-Ia³, unc-5⁸ has motor neuron phenotype, non-enhanceable by Nrg^l10

(Zarin et al., 2014)

Suppressed by

Statement

Reference

unc-5⁸ has embryonic heart cardioblast phenotype, suppressible | partially by robo1¹/robo1[+]

(Raza and Jacobs, 2016)

NOT suppressed by

Statement

Reference

beat-Ia^C163/beat-Ia³, unc-5⁸ has motor neuron phenotype, non-suppressible by Nrg^l10

(Zarin et al., 2014)

Enhancer of

Statement

Reference

unc-5[+]/unc-5⁸ is an enhancer of embryonic heart cardioblast | embryonic stage phenotype of robo1¹

(Raza and Jacobs, 2016)

unc-5[+]/unc-5⁸ is an enhancer of filopodium | embryonic stage phenotype of robo1¹

(Raza and Jacobs, 2016)

unc-5[+]/unc-5⁸ is an enhancer of lamellipodium | embryonic stage phenotype of robo1¹

(Raza and Jacobs, 2016)

unc-5[+], beat-Ia[+], unc-5⁸, beat-Ia³ is an enhancer of larval intersegmental nerve phenotype of eve^ΔRP2A

(Zarin et al., 2014)

unc-5[+]/unc-5⁸ is an enhancer of larval intersegmental nerve phenotype of eve³

(Zarin et al., 2014)

unc-5[+], beat-Ia^C163, beat-Ia[+], unc-5⁸ is an enhancer of larval intersegmental nerve phenotype of eve³

(Zarin et al., 2014)

Suppressor of

Statement

Reference

unc-5⁸ is a suppressor of eye phenotype of Hsap\UBQLN2^P4X.UAS, Scer\GAL4^GMR.PU

(Kim et al., 2023)

unc-5[+]/unc-5⁸ is a suppressor of embryonic heart cardioblast | embryonic stage phenotype of robo1¹

(Raza and Jacobs, 2016)

unc-5⁸ is a suppressor | partially of larval EW neuron phenotype of Scer\GAL4^eg-Mz360, eve^UAS.cBa

(Zarin et al., 2014)

beat-Ia^C163, unc-5⁸, beat-Ia³ is a suppressor | partially of larval EW neuron phenotype of Scer\GAL4^eg-Mz360, eve^UAS.cBa

(Zarin et al., 2014)

Other

Statement

Reference

grn^7L, unc-5[+]/unc-5⁸ has larval intersegmental nerve phenotype

(Zarin et al., 2012)

Df(2R)eve, eve^ΔRP2A, unc-5⁸ has larval intersegmental nerve phenotype

(Zarin et al., 2012)

Additional Comments

Genetic Interactions

Statement

Reference

unc-5⁸, robo1¹ double heterozygotes show a less severe decrease in migration velocity compared to either single heterozygote conditions, a more severe decrease in filopodial activity compared to either single heterozygote conditions, and a more severe decrease in lamellopodial activity compared to robo1¹ heterozygotes.

(Raza and Jacobs, 2016)

CNS exit from EW neurons misexpressing eve^Scer\UAS.cBa is partially suppressed in an unc-5⁸ mutant background and midline crossing is partially restored.

CNS exit from EW neurons misexpressing eve^Scer\UAS.cBa is partially suppressed in an unc-5⁸ beat-Ia^C163/beat-Ia³ mutant background while midline crossing is partially restored (in 15% of hemisegments).

Nrg^l10; unc-5⁸ double mutants exhibit aberrant motorneuron crossing to the adjacent segment before the first branch point. The number of late defects is also substantially increased compared to both single mutants.

Nrg^l10/Y; unc-5⁸, beat-Ia^C163/beat-Ia³ triple mutants exhibit severe defects in the intersegmental nerve crossing in the ventral muscle field.

unc-5⁸, beat-Ia^C163/beat-Ia³ mutants exhibit a failure of motor neurons to exit the CNS in 10% of hemisegments.

The addition of a Nrg^l10/Y background does not affect the unc-5⁸, beat-Ia^C163/beat-Ia³ CNS exit failure seen in 10% of unc-5⁸, beat-Ia^C163/beat-Ia³ hemisegments.

A transheterozygous combination of eve^ΔRP2A/+, unc-5⁸/+ reduces beat-Ia levels to 50% and significantly increases the defects seen in intersegmental nerves, with the number of axons that exhibit stalling increasing from 3% to 7.5% in eve^ΔRP2A/+, unc-5⁸/+ transheterozygotes and eve^ΔRP2A/+, unc-5⁸/+, beat-Ia³/+ triple heterozygotes, respectively.

A transheterozygous combination of eve³/+, unc-5⁸/+ reduces beat-Ia levels to 50% and significantly increases the defects seen in intersegmental nerves, with the number of axons exhibiting stalling increasing from 8.1% to 23.1% in eve³/+, unc-5⁸/+ transheterozygotes and eve³/+, unc-5⁸/+, beat-Ia^C163/+ triple heterozygotes, respectively.

(Zarin et al., 2014)

eve^ΔRP2A, Df(2R)eve/+ ; unc-5⁸/+ double heterozygous embryos show guidance defects in the intersegmental nerve.

unc-5⁸/+ ; grn^7L/+ double heterozygous embryos show guidance defects in the intersegmental nerve.

(Zarin et al., 2012)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

unc-5⁸ is rescued by unc-5^{UAS.Tag:HA,Tag:SS(wg)}/Scer\GAL4^Mef2.247

(Raza and Jacobs, 2016)

Partially rescued by

unc-5⁸ is partially rescued by unc-5^{UAS.Tag:HA,Tag:SS(wg)}/Scer\GAL4^cas-3921

(von Hilchen et al., 2010)

unc-5⁸ is partially rescued by unc-5^{UAS.Tag:HA,Tag:SS(wg)}/Scer\GAL4^repo

(von Hilchen et al., 2010)

unc-5⁸/unc-5² is partially rescued by unc-5^{UAS.Tag:HA,Tag:SS(wg)}/Scer\GAL4^elav.PLu

(Labrador, 2005)

Comments

The unc-5⁸ homozygous embryonic heart cardioblast defects (i.e. migration velocity and in filopodial and lamellopodial extensions and activities) and embryonic heart lumen formation defects are rescued by the expression of unc-5^{Scer\UAS.T:Ivir\HA1,T:SS-wg} under the control of Scer\GAL4^Mef2.247.

(Raza and Jacobs, 2016)

Expression of unc-5^{Scer\UAS.T:Ivir\HA1,T:SS-wg} under the control of Scer\GAL4^cas-3921 in unc-5⁸ embryos rescues the normal number of six embryonic peripheral glia distal to the SNc in 49% of hemisegments (compared to only 6% of hemisegments in unc-5⁸ embryos) and five ePG are found distal to the SNc in 39% of hemisegments (compared to only 24% of hemisegments in unc-5⁸ embryos).

Expression of unc-5^{Scer\UAS.T:Ivir\HA1,T:SS-wg} under the control of Scer\GAL4^repo in unc-5⁸ embryos rescues the normal number of six embryonic peripheral glia distal to the SNc in 49% of hemisegments (compared to only 6% of hemisegments in unc-5⁸ embryos) and five ePG are found distal to the SNc in 33% of hemisegments (compared to only 24% of hemisegments in unc-5⁸ embryos).

(von Hilchen et al., 2010)

Expression of unc-5^{Scer\UAS.T:Ivir\HA1,T:wg}, under the control of Scer\GAL4^elav.PLu, partially rescues the ISN and SNa defects of unc-5²/unc-5⁸ mutants.

(Labrador, 2005)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

Selected as: a suppressor of the unc-5^GS; Scer\GAL4^scrt-GAL4 lethal phenotype.

(Labrador, 2005)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (3)

Reported As

Symbol Synonym

Unc-5⁸

(Kim et al., 2023, Zarin et al., 2014, Labrador, 2005)

unc-5⁸

(Zarin et al., 2012)

unc5⁸

(Raza and Jacobs, 2016, von Hilchen et al., 2010)

Name Synonyms

Secondary FlyBase IDs

References (6)

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