FlyBase Allele Report: Dmel\comm[1]

General Information

Symbol

Dmel\comm¹

Species

D. melanogaster

Name

FlyBase ID

FBal0030916

Feature type

allele

Associated gene

Dmel\comm

Associated Insertion(s)

Carried in Construct

Key Links

Genomic Maps

JBrowse

Allele class

hypomorphic allele - genetic evidence

Mutagen

ethyl methanesulfonate

Nature of the Allele

Allele class

hypomorphic allele - genetic evidence

(Tear et al., 1996)

Mutagen

ethyl methanesulfonate

(Tear et al., 1996, Seeger et al., 1993)

Progenitor genotype

Cytology

Description

Frameshift mutation at amino acid 217, resulting in a premature termination following 26 amino acids of the novel reading frame.

(Tear et al., 1996)

Mutations Mapped to the Genome

Curation Data

Type

Location

Additional Notes

References

delins

3L:15,723,123..15,723,131 [-]

Comment:

comm¹ is a deletion of 9bp with an insertion of 2bp, causing a frameshift at amino acid 217. This leads to premature translation termination after the addtion of 26 novel amino acids. The annotated deletion endpoints are approximate.

(Tear et al., 1996)

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

(Hsouna et al., 2003, Georgiou and Tear, 2002, Kim et al., 2002, Myat et al., 2002)

abnormal neuroanatomy (with comm⁵)

(Wolf et al., 1998)

abnormal neuroanatomy | recessive

(Wolf et al., 1998)

lethal | recessive

(Tear et al., 1996)

uncoordinated

(Tear et al., 1996)

Phenotype Manifest In

Detailed Description

Statement

Reference

Commissural axons are prevented from forming in comm¹ mutants.

(Hsouna et al., 2003)

Mitotically recombined neuronal clones homozygous for comm¹ cross the ventral midline in 70% of cases, compared to 85% of cases in wild-type samples.

(McGovern and Seeger, 2003)

The commissures form in 21.9% of mutant embryos, although commissure formation is usually restricted to one or two thoracic segments.

(Georgiou and Tear, 2002)

The commissures are almost all absent in homozygous embryos, with axons only crossing the midline in about 9% of embryos.

(Kim et al., 2002)

All commissural axons fail to cross the midline.

(Myat et al., 2002)

comm¹ mutants have a commissureless phenotype.

(Bashaw et al., 2000)

The motoneuron growth cones fail to initiate synaptogenesis on contacting their target muscles in homozygous or comm¹/comm⁵ embryos. The axons either stall just short of synaptic targets or they extend beyond the normal stopping points without apparently settling on alternative targets. These phenotypes are seen in the five motoneuron nerve groups (the ISN, SNa, SNb, SNc and SNd).

(Wolf et al., 1998)

Strong allele. Commissures are not completely absent but partial and highly abnormal commissures form. Rare adult escapers of hypomorphic allelic combinations show a range of uncoordinated behaviors.

(Tear et al., 1996)

Commissural axons rarely cross the midline of the VNC, so the midline glia have minimal contact with axons. Temporal pattern of midline glial death correlates with a 39% decrease in numbers from stage 13 to stage 17 of embryogenesis, relative to a 21% decrease over the same period for wild type.

(Sonnenfeld and Jacobs, 1995)

All commissural pathways are lacking, while other axon pathways appear normal. Differentiation of the brain commissure, involving the projection of many axons across the midline and formation of additional commissural fascicles, does not take place. As a result the brain commissure is greatly reduced.

(Therianos et al., 1995)

Commissural axon pathways in the embryonic ventral nerve cord absent.

(Seeger et al., 1993)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Suppressed by

Statement

Reference

comm¹ has abnormal neuroanatomy phenotype, suppressible by Abl^UAS.cHa/Scer\GAL4^ftz.ng

(Hsouna et al., 2003)

comm¹ has abnormal neuroanatomy phenotype, suppressible by Abl^UAS.cHa/Scer\GAL4^elav.PLu

(Hsouna et al., 2003)

comm¹ has abnormal neuroanatomy phenotype, suppressible by Abl^KN.UAS/Scer\GAL4^elav.PLu

(Hsouna et al., 2003)

comm¹ has abnormal neuroanatomy phenotype, suppressible by Abl^KN.UAS/Scer\GAL4^ftz.ng

(Hsouna et al., 2003)

comm¹ has abnormal neuroanatomy phenotype, suppressible by Scer\GAL4^elav.PLu/Abl::Hsap\ABL1::Hsap\BCR^P210.UAS

(Hsouna et al., 2003)

comm¹ has abnormal neuroanatomy phenotype, suppressible by Abl::Hsap\ABL1::Hsap\BCR^P210.UAS/Scer\GAL4^ftz.ng

(Hsouna et al., 2003)

comm¹ has abnormal neuroanatomy phenotype, suppressible by Ggal\MLCK^ct.UAS/Scer\GAL4^elav.PLu

(Kim et al., 2002)

comm¹ has abnormal neuroanatomy phenotype, suppressible by Ggal\MLCK^ct.UAS/Scer\GAL4^ftz.ng

(Kim et al., 2002)

Phenotype Manifest In

NOT Enhanced by

Statement

Reference

comm¹ has larval ventral nerve cord commissure phenotype, non-enhanceable by robo2⁵

(Rajagopalan et al., 2000)

Suppressed by

Statement

Reference

comm¹ has symmetrical commissure phenotype, suppressible by Abl^KN.UAS/Scer\GAL4^ftz.ng

(Hsouna et al., 2003)

comm¹ has symmetrical commissure phenotype, suppressible by Abl::Hsap\ABL1::Hsap\BCR^P210.UAS/Scer\GAL4^ftz.ng

(Hsouna et al., 2003)

comm¹ has symmetrical commissure phenotype, suppressible by Scer\GAL4^elav.PLu/Abl::Hsap\ABL1::Hsap\BCR^P210.UAS

(Hsouna et al., 2003)

comm¹ has symmetrical commissure phenotype, suppressible by Abl^UAS.cHa/Scer\GAL4^ftz.ng

(Hsouna et al., 2003)

comm¹ has symmetrical commissure phenotype, suppressible by Abl^UAS.cHa/Scer\GAL4^elav.PLu

(Hsouna et al., 2003)

comm¹ has symmetrical commissure phenotype, suppressible by Abl^KN.UAS/Scer\GAL4^elav.PLu

(Hsouna et al., 2003)

comm¹ has symmetrical commissure phenotype, suppressible by Ggal\MLCK^ct.UAS/Scer\GAL4^elav.PLu

(Kim et al., 2002)

comm¹ has symmetrical commissure phenotype, suppressible by Ggal\MLCK^ct.UAS/Scer\GAL4^ftz.ng

(Kim et al., 2002)

comm¹ has symmetrical commissure phenotype, suppressible by ena^GC1

(Bashaw et al., 2000)

NOT suppressed by

Statement

Reference

comm¹ has larval ventral nerve cord commissure phenotype, non-suppressible by robo2⁵

(Rajagopalan et al., 2000)

NOT Suppressor of

Statement

Reference

comm¹ is a non-suppressor of larval ventral nerve cord phenotype of robo1¹, robo2⁵

(Rajagopalan et al., 2000)

Additional Comments

Genetic Interactions

Statement

Reference

Using Scer\GAL4^ftz.ng, expression of Abl^Scer\UAS.cHa in a subset of neurons in a comm¹ background causes a few thin commissures to reform.

Pan-neural expression of Abl^Scer\UAS.cHa under the control of Scer\GAL4^elav.PLu partially suppresses the comm¹ commissure phenotype.

Pan-neural expression of Abl^KN.Scer\UAS under the control of Scer\GAL4^elav.PLu partially suppresses the comm¹ commissure phenotype.

Expression of Abl^KN.Scer\UAS in a subset of neurons under the control of Scer\GAL4^ftz.ng partially suppresses the comm¹ commissure phenotype.

(Hsouna et al., 2003)

The addition of lea^robo2-5 to comm¹ embryos has no effect on the number of commissures crossing the midline in the ventral nerve cords in these mutants. The addition of comm¹ to robo¹, lea^robo2-5 embryos has no effect on the ventral nerve cord phenotype.

(Rajagopalan et al., 2000)

Xenogenetic Interactions

Statement

Reference

Pan-neural expression of Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS} under the control of Scer\GAL4^elav.PLu partially suppresses the comm¹ commissure phenotype.

Expression of Abl::Hsap\ABL1::Hsap\BCR^{P210.Scer\UAS} in a subset of neurons under the control of Scer\GAL4^ftz.ng partially suppresses the comm¹ commissure phenotype.

(Hsouna et al., 2003)

Expression of Ggal\MLCK^ct.Scer\UAS under the control of Scer\GAL4^ftz.ng in comm¹ embryos results in 49% of embryos showing some axons crossing the midline and in many cases thin commissures are present. Expression of Ggal\MLCK^ct.Scer\UAS under the control of Scer\GAL4^elav.PLu in comm¹ embryos results in partial commissure formation in 71% of embryos.

(Kim et al., 2002)

Complementation and Rescue Data

Partially rescued by

comm¹ is partially rescued by comm^UAS.cKa/Scer\GAL4^sim.P3.7

(Georgiou and Tear, 2002)

comm¹ is partially rescued by comm^UAS.cKa/Scer\GAL4^sli.PS

(Georgiou and Tear, 2002)

Comments

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

comm¹

(Hsouna et al., 2003)

comm^A490

(Georgiou and Tear, 2002)

Name Synonyms

Secondary FlyBase IDs

References (12)

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