FlyBase Allele Report: Dmel\beat-Ia[3]

General Information

Symbol

Dmel\beat-Ia³

Species

D. melanogaster

Name

FlyBase ID

FBal0057747

Feature type

allele

Associated gene

Dmel\beat-Ia

Associated Insertion(s)

Carried in Construct

Also Known As

beat³

Key Links

Genomic Maps

JBrowse

Allele class

loss of function allele

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

loss of function allele

(Fambrough and Goodman, 1996)

Mutagen

ethyl methanesulfonate

(Ashburner et al., 1999.10.12, Fambrough and Goodman, 1996)

Progenitor genotype

Cytology

Description

Amino acid replacement: K235term.

(Heymann et al., 2022)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

point_mutation

2L:16,080,037..16,080,037 [+]

Nucleotide change:

A16080037T

Amino acid change:

K235term | beat-Ia-PA; K235term | beat-Ia-PB

Reported amino acid change:

K235term

Comment:

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

(Heymann et al., 2022)

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

Bolwig organ

(Holmes and Heilig, 1999)

larval abdominal intersegmental nerve

(Kaufmann et al., 1998)

larval abdominal segmental nerve

(Fambrough and Goodman, 1996)

motor neuron

(Fambrough and Goodman, 1996)

muscle cell of A1-7 dorsal acute muscle 1 (with beat-Ia^C163)

(Siebert et al., 2009)

muscle cell of A1-7 dorsal acute muscle 2 (with beat-Ia^C163)

(Siebert et al., 2009)

muscle cell of A1-7 dorsal oblique muscle 1 (with beat-Ia^C163)

(Siebert et al., 2009)

muscle cell of A1-7 dorsal oblique muscle 2 (with beat-Ia^C163)

(Siebert et al., 2009)

muscle cell of A1-7 ventral longitudinal muscle 1 (with beat-Ia^C163)

(Siebert et al., 2009)

muscle cell of A1-7 ventral longitudinal muscle 2 (with beat-Ia^C163)

(Siebert et al., 2009)

muscle cell of A1-7 ventral longitudinal muscle 3 (with beat-Ia^C163)

(Siebert et al., 2009)

muscle cell of A1-7 ventral longitudinal muscle 4 (with beat-Ia^C163)

(Siebert et al., 2009)

photoreceptor

(Holmes and Heilig, 1999)

Detailed Description

Statement

Reference

beat-Ia³/beat-Ia^C163 third instar larvae often lack neuromuscular junctions (NMJs) on dorsal muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 1 (31%), muscle 9 (34%), muscle 2 (8%), muscle 10 (13%).

beat-Ia³/beat-Ia^C163 third instar larvae often lack neuromuscular junctions (NMJs) on ventral muscles (the percentage of muscles lacking NMJs is given in parentheses); muscle 12 (25%), muscle 13 (34%), muscle 6 (38%), muscle 7 (55%).

(Siebert et al., 2009)

Cells of the Bolwig's organs (BOs) form in homozygous embryos, but the morphology of the larval visual system (LVS) is severely disrupted and increased numbers of photoreceptor cells are apparent from the earliest stages of LVS development. Extra photoreceptor cells are seen both in the normal location of the BO clusters and dispersed between the two clusters. Embryos sometimes contain three BO's and, rarely, four BO clusters are seen. Migration of the BOs appears relatively normal in some embryos, but in others it is disrupted and the BO does not achieve its proper location even though head involution appears normal, or the BO is elongated.

(Holmes and Heilig, 1999)

Motor axons exit the CNS normally but then fail to branch and enter their muscle domains once in the periphery. The SNb fails to diverge from the ISN either completely (full bypass), 45% segments, or partially (partial bypass), 39% segments, the SNc fails to diverge in 77% segments.

(Fambrough and Goodman, 1996)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

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)

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

beat-Ia^C163, Nrg^l10, beat-Ia³ is an enhancer of abnormal neuroanatomy phenotype of unc-5⁸

(Zarin et al., 2014)

beat-Ia^C163/beat-Ia³ is an enhancer of abnormal neuroanatomy phenotype of unc-5⁸

(Zarin et al., 2014)

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

(Zarin et al., 2014)

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

(Zarin et al., 2014)

Suppressor of

Statement

Reference

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

SoxN^GA1192, beat-Ia[+]/beat-Ia³ has partially lethal - majority die phenotype

(Girard et al., 2006)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

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

(Zarin et al., 2014)

beat-Ia^C163/beat-Ia³ has muscle cell of A1-7 dorsal acute muscle 1 phenotype, non-enhanceable by Scer\GAL4^how-24B

(Siebert et al., 2009)

beat-Ia^C163/beat-Ia³ has muscle cell of A1-7 dorsal acute muscle 2 phenotype, non-enhanceable by Scer\GAL4^how-24B

(Siebert et al., 2009)

beat-Ia^C163/beat-Ia³ has muscle cell of A1-7 dorsal oblique muscle 1 phenotype, non-enhanceable by Scer\GAL4^how-24B

(Siebert et al., 2009)

beat-Ia^C163/beat-Ia³ has muscle cell of A1-7 dorsal oblique muscle 2 phenotype, non-enhanceable by Scer\GAL4^how-24B

(Siebert et al., 2009)

beat-Ia^C163/beat-Ia³ has muscle cell of A1-7 dorsal acute muscle 1 phenotype, non-enhanceable by Scer\GAL4^Mef2.PR

(Siebert et al., 2009)

beat-Ia^C163/beat-Ia³ has muscle cell of A1-7 dorsal acute muscle 2 phenotype, non-enhanceable by Scer\GAL4^Mef2.PR

(Siebert et al., 2009)

beat-Ia^C163/beat-Ia³ has muscle cell of A1-7 dorsal oblique muscle 1 phenotype, non-enhanceable by Scer\GAL4^Mef2.PR

(Siebert et al., 2009)

beat-Ia^C163/beat-Ia³ has muscle cell of A1-7 dorsal oblique muscle 2 phenotype, non-enhanceable by Scer\GAL4^Mef2.PR

(Siebert et al., 2009)

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

beat-Ia^C163, Nrg^l10, beat-Ia³ is an enhancer of larval intersegmental nerve phenotype of unc-5⁸

(Zarin et al., 2014)

beat-Ia^C163/beat-Ia³ is an enhancer of motor neuron phenotype of unc-5⁸

(Zarin et al., 2014)

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

(Zarin et al., 2014)

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

(Zarin et al., 2014)

Suppressor of

Statement

Reference

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

SoxN^GA1192, beat-Ia[+]/beat-Ia³ has larval longitudinal connective phenotype

(Girard et al., 2006)

SoxN^GA1192, beat-Ia[+]/beat-Ia³ has larval anterior commissure phenotype

(Girard et al., 2006)

SoxN^GA1192, beat-Ia[+]/beat-Ia³ has larval posterior commissure phenotype

(Girard et al., 2006)

Additional Comments

Genetic Interactions

Statement

Reference

Nrg^l10/Y; beat-Ia^C163/beat-Ia³ double mutants exhibit intersegmental nerve axon stalling prior to the first branch point.

unc-5⁸, beat-Ia^C163/beat-Ia³ double mutants exhibit intersegmental nerve axon stalling prior to the first branch point.

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.

Nrg^l10/Y; beat-Ia^C163/beat-Ia³ double mutants do not exhibit any aCC or RP2 exit phenotypes.

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.

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).

(Zarin et al., 2014)

The neuromuscular junction innervation defects seen in the dorsal muscles of beat-Ia³/beat-Ia^C163 third instar larvae are not enhanced by expression of side^Scer\UAS.cSa under the control of either Scer\GAL4^how-24B or Scer\GAL4^Mef2.PR.

(Siebert et al., 2009)

beat-Ia/+, SoxN^GA1192/+ double heterozygous embryos commissures are partially fused and the longitudinal connectives are thinner or missing. This phenotype is not seen in either beat-Ia/+ or SoxN^GA1192/+ embryos.

(Girard et al., 2006)

beat-Ia²/beat-Ia³ Rac1^N17.Scer\UAS Scer\GAL4^elav-C155 double mutant embryos exhibit additive, not synergistic effects on the ISNb full bypass phenotype.

(Kaufmann et al., 1998)

In beat-Ia²/beat-Ia³ transheterozygotes the SNb fails to diverge from the ISN completely (full bypass) in 38% segments or partially (partial bypass) in 28% segments. The SNb divergence defect can be suppressed by Fas2^e76 and the SNc defect by Con^Fvex238.

(Fambrough and Goodman, 1996)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Rescued by

beat-Ia^C163/beat-Ia³ is rescued by beat-Ia^UAS.cFa/Scer\GAL4^elav.PLu

(Siebert et al., 2009)

beat-Ia^C163/beat-Ia³ is rescued by beat-Ia^UAS.cFa/Scer\GAL4^Fas2-Mz507

(Siebert et al., 2009)

beat-Ia³ is rescued by Scer\GAL4^elav-C155/beat-Ia^UAS.cFa

(Fambrough and Goodman, 1996)

Not rescued by

beat-Ia^C163/beat-Ia³ is not rescued by beat-Ia^UAS.cFa/Scer\GAL4^Mef2.PR

(Siebert et al., 2009)

Comments

Scer\GAL4^elav-C155 mediated expression of beat-Ia^Scer\UAS.cFa rescues the SNb divergence defect.

(Fambrough and Goodman, 1996)

Images (0)

Mutant

Wild-type

Stocks (1)

Bloomington

4748

w^*; beat-Ia³ Fas3^E25/CyO, P{act-lacZ.B}CB1

Notes on Origin

Discoverer

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (4)

Reported As

Symbol Synonym

Beat-Ia³

(Talsma et al., 2014)

beat Ia³

(Zarin et al., 2014)

beat-Ia³

(Fabre et al., 2010, Girard et al., 2006)

beat³

(Heymann et al., 2022, Kinold et al., 2018, Siebert et al., 2009, Ashburner et al., 1999.10.12, Holmes and Heilig, 1999, Kaufmann et al., 1998, Fambrough and Goodman, 1996)

Name Synonyms

Secondary FlyBase IDs

References (11)

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