FlyBase Allele Report: Dmel\Sema2a[03474]

General Information

Symbol

Dmel\Sema2a⁰³⁴⁷⁴

Species

D. melanogaster

Name

FlyBase ID

FBal0028553

Feature type

allele

Associated gene

Dmel\Sema2a

Associated Insertion(s)

P{PZ}Sema2a⁰³⁴⁷⁴

Carried in Construct

Also Known As

SemaII^P2, sema-2a^P2

Key Links

Allele class

loss of function allele

Mutagen

Nature of the Allele

Allele class

loss of function allele

(Kolodkin et al., 1993)

Mutagen

P-element activity

Delta2-3 transposase

(Kolodkin et al., 1993)

Progenitor genotype

Associated Insertion(s)

P{PZ}Sema2a⁰³⁴⁷⁴

Cytology

Description

P element inserted 600bp upstream of the longest semaII cDNA clone, which is not complete.

(Kolodkin et al., 1993)

Allele components

Component

Use(s)

Inserted element

P{PZ}

enhancer trap

Encoded product / tool

lacZ

reporter enzyme

Tagged with

Tag:NLS(P)

nuclear protein localization tag

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 behavior | recessive

(Kolodkin et al., 1993)

abnormal neuroanatomy

(Bates and Whitington, 2007)

abnormal neuroanatomy (with Sema2a^ex59)

(Bates and Whitington, 2007)

flightless | recessive

(Kolodkin et al., 1993)

lethal | recessive

(Kolodkin et al., 1993)

Phenotype Manifest In

abdominal lateral oblique muscle 1 & neuromuscular junction

(Winberg et al., 1998)

abdominal segment border muscle & neuromuscular junction

(Winberg et al., 1998)

abdominal ventral longitudinal muscle 2 & neuromuscular junction

(Winberg et al., 1998)

abdominal ventral longitudinal muscle 3 & neuromuscular junction

(Winberg et al., 1998)

abdominal ventral longitudinal muscle 4 & neuromuscular junction

(Winberg et al., 1998)

embryonic/larval salivary gland | embryonic stage (with Sema2a^k11240)

(Hanlon and Andrew, 2016)

larval abdominal segmental nerve

(Winberg et al., 1998)

larval intersegmental nerve

(Winberg et al., 1998)

larval transverse nerve

(Winberg et al., 1998)

lch1 neuron

(Bates and Whitington, 2007)

lch1 neuron (with Sema2a^ex59)

(Bates and Whitington, 2007)

lobula columnar neuron LC14

(Bates and Whitington, 2007)

lobula columnar neuron LC14 (with Sema2a^ex59)

(Bates and Whitington, 2007)

neuromuscular junction | ectopic

(Winberg et al., 1998)

Detailed Description

Statement

Reference

Sema2a⁰³⁴⁷⁴/Sema2a^k11240 transheterozygous embryos show high frequency of defects in the salivary gland (SG) lumen (the distal end of the SG which normally contacts the VIS5 muscle is often directed away from the muscle) compared to wild-type controls.

(Hanlon and Andrew, 2016)

DL1 and VM2 projection neuron dendrites target normally to the dorsolateral DL1 glomerulus in homozygous flies.

(Sweeney et al., 2011)

Approximately 14.6% of homozygous Sema-2a⁰³⁰²¹ hemisegments exhibit abnormal v'ch1 projection, with the axon mis-projecting anteriorly and joining the inter-segmental nerve instead of the segmental nerve. In most cases of v'ch1 mis-projection, the axon contacts the cell bodies and axons of nearby lateral cluster neurons, lesA and 1daA, which are located anterior and slightly internal to the v'ch1 cell body. In a small number of defective hemisegments, the v'ch1 axon bifuricates sending its axon both anteriorly to the intersegmental nerve and ventrally to join the segmental nerve. Mis-projections of dorsal cluster sensory neurons are also observed in homozygous Sema-2a⁰³⁰²¹ mutants. One or more axons of dorsal cluster neurons either mis-projects posteriorly or loops anteriorly in the dorsal region before joining the intersegmental nerve in its normal position in the lateral region.

Approximately 18.3% of Sema-2a⁰³⁴⁷⁴/Sema-2a^ex59 hemisegments exhibit abnormal v'ch1 projection, with the axon mis-projecting anteriorly and joining the inter-segmental nerve instead of the segmental nerve. In most cases of v'ch1 mis-projection, the axon contacts the cell bodies and axons of nearby lateral cluster neurons, lesA and 1daA, which are located anterior and slightly internal to the v'ch1 cell body. In a small number of defective hemisegments, the v'ch1 axon bifuricates sending its axon both anteriorly to the intersegmental nerve and ventrally to join the segmental nerve.

(Bates and Whitington, 2007)

The ISNb makes normal contact with muscle 12 and then extends ectopic connections dorsally and laterally into muscle 8. Ectopic connections are also observed for the transverse nerve into ventral muscles 7,6 or 13. The SNa stops abruptly at muscle 5, does not innervate muscle 8 but makes increased contact with muscle 5.

(Winberg et al., 1998)

Eclosion of adults is greatly reduced, and eclosed adults show flightlessness and behavioral defects in drinking tests and visual orientation tests though they are not blind. They survive for only 2 days. At the gross structural level there are no abnormalities in patterning of CNS and PNS axon tracts, nor in the brain neuropil of the adult.

(Kolodkin et al., 1993)

External Data

Linkouts

Interactions

Show genetic interaction network for Enhancers & Suppressors

Phenotypic Class

Enhanced by

Statement

Reference

Sema2a⁰³⁴⁷⁴ has abnormal neuroanatomy phenotype, enhanceable by PlexB^KG00878

(Bates and Whitington, 2007)

Sema2a⁰³⁴⁷⁴ has abnormal neuroanatomy phenotype, enhanceable by Df(4)C3

(Bates and Whitington, 2007)

NOT Enhancer of

Statement

Reference

Sema2a⁰³⁴⁷⁴/Df(2R)A15 is a non-enhancer of abnormal neuroanatomy phenotype of Sema2b^f02042

(Meltzer et al., 2016)

Other

Statement

Reference

Scer\GAL4^peb-GAL4, Scer\GAL80^Orco, Sema2a⁰³⁴⁷⁴, Sema2b^3'UTR.UAS, Sema2b^f02042 has abnormal neuroanatomy phenotype

(Joo et al., 2013)

Sema2a⁰³⁴⁷⁴, Sema2b^f02042 has abnormal neuroanatomy phenotype

(Joo et al., 2013)

Sema-2a[+]/Sema2a⁰³⁴⁷⁴, Sema2b^unspecified has abnormal neuroanatomy | adult stage phenotype

(Sweeney et al., 2011)

Scer\GAL4^peb-GAL4, Sema-2a[+]/Sema2a⁰³⁴⁷⁴, Sema2a^GD5476, Sema2b^unspecified has abnormal neuroanatomy | adult stage phenotype

(Sweeney et al., 2011)

Sema2a⁰³⁴⁷⁴, Sema2b^unspecified has abnormal neuroanatomy | adult stage phenotype

(Sweeney et al., 2011)

Sema2a⁰³⁴⁷⁴, Sema2b^unspecified has abnormal neuroanatomy | somatic clone | adult stage phenotype

(Sweeney et al., 2011)

Phenotype Manifest In

Enhanced by

Statement

Reference

Sema2a⁰³⁴⁷⁴ has lch1 neuron phenotype, enhanceable by PlexB^KG00878

(Bates and Whitington, 2007)

Sema2a⁰³⁴⁷⁴ has lch1 neuron phenotype, enhanceable by Df(4)C3

(Bates and Whitington, 2007)

Enhancer of

Statement

Reference

Sema2a⁰³⁴⁷⁴ is an enhancer of larval transverse nerve phenotype of Fas2^UAS.cLb, Scer\GAL4^l(3)H94-H94

(Winberg et al., 1998)

NOT Enhancer of

Statement

Reference

Sema2a⁰³⁴⁷⁴/Df(2R)A15 is a non-enhancer of larval multidendritic class IV neuron | third instar larval stage phenotype of Sema2b^f02042

(Meltzer et al., 2016)

Other

Statement

Reference

Scer\GAL4^peb-GAL4, Scer\GAL80^Orco, Sema2a⁰³⁴⁷⁴, Sema2b^3'UTR.UAS, Sema2b^f02042 has adult brain phenotype

(Joo et al., 2013)

Scer\GAL4^peb-GAL4, Scer\GAL80^Orco, Sema2a⁰³⁴⁷⁴, Sema2b^3'UTR.UAS, Sema2b^f02042 has antennal lobe phenotype

(Joo et al., 2013)

Scer\GAL4^peb-GAL4, Scer\GAL80^Orco, Sema2a⁰³⁴⁷⁴, Sema2b^3'UTR.UAS, Sema2b^f02042 has adult olfactory receptor neuron phenotype

(Joo et al., 2013)

Sema2a⁰³⁴⁷⁴, Sema2b^f02042 has adult brain phenotype

(Joo et al., 2013)

Sema2a⁰³⁴⁷⁴, Sema2b^f02042 has antennal lobe phenotype

(Joo et al., 2013)

Sema2a⁰³⁴⁷⁴, Sema2b^f02042 has adult olfactory receptor neuron phenotype

(Joo et al., 2013)

Sema2a⁰³⁴⁷⁴, Sema2b^unspecified has adult antennal lobe projection neuron VM2 adPN phenotype

(Sweeney et al., 2011)

Sema2a⁰³⁴⁷⁴, Sema2b^unspecified has adult antennal lobe phenotype

(Sweeney et al., 2011)

Sema2a⁰³⁴⁷⁴, Sema2b^unspecified has adult antennal lobe projection neuron VA1d adPN phenotype

(Sweeney et al., 2011)

Sema-2a[+]/Sema2a⁰³⁴⁷⁴, Sema2b^unspecified has adult antennal lobe projection neuron phenotype

(Sweeney et al., 2011)

Scer\GAL4^peb-GAL4, Sema-2a[+]/Sema2a⁰³⁴⁷⁴, Sema2a^GD5476, Sema2b^unspecified has adult antennal lobe projection neuron phenotype

(Sweeney et al., 2011)

Sema2a⁰³⁴⁷⁴, Sema2b^unspecified has adult antennal lobe projection neuron VM2 adPN | somatic clone phenotype

(Sweeney et al., 2011)

Sema2a⁰³⁴⁷⁴, Sema2b^unspecified has adult antennal lobe projection neuron DL1 adPN phenotype

(Sweeney et al., 2011)

NetB^UAS.cHa, Scer\GAL4^how-24B, Sema2a⁰³⁴⁷⁴ has larval segmental nerve phenotype

(Winberg et al., 1998)

NetB^UAS.cHa, Scer\GAL4^how-24B, Sema2a⁰³⁴⁷⁴ has larval abdominal segmental nerve phenotype

(Winberg et al., 1998)

Additional Comments

Genetic Interactions

Statement

Reference

The increased dendritic non-contacting crossing in the class IV dendritic arborizing neurons seen in Sema-2b^f02042 mutant larvae is not enhanced by the loss of Sema-2a : Sema-2b^f02042,Sema-2a⁰³⁴⁷⁴/Df(2R)A15 mutant larvae display the same amount of dendrite self-crossing as Sema-2b^f02042 mutants alone.

(Meltzer et al., 2016)

Sema-2a⁰³⁴⁷⁴ Sema-2b^f02042 double homozygous mutants exhibit ORN axon trajectory defects, with most axons projecting dorsolaterally. Expression of Sema-2b^{3'UTR.Scer\UAS} in adult ORNs, under the control of Scer\GAL4^peb-GAL4 and Scer\GAL80^Orco, in these double mutants leads to Sema-2b-expressing ORNS exhibiting three kinds of trajectory. In 15% of cases, axons are split between the dorsolateral and ventromedial trajectories. In the remaining 85% of cases, however, all axons exclusively chose either the ventromedial or dorsolateral trajectory, with nearly equal probability.

(Joo et al., 2013)

Overall antennal lobe morphology is disrupted in Sema-2a⁰³⁴⁷⁴ Sema-2b^unspecified double homozygous flies. Dendrite targeting defects are seen for a number of projection neurons. The dendrites of the DL1 projection neurons are either split between the DL1 glomerulus (wild-type target) and an ectopic ventromedial position or entirely shifted ventromedially. DL3 projection neuron dendrites mistarget ventrally or ventromedially. VA1d and DA1 projection neuron dendrites mistarget ventromedially and ventrolaterally. VM2 projection neuron dendrites show significant dorsolateral mistargeting.

Sema-2a⁰³⁴⁷⁴/+ Sema-2b^unspecified/Sema-2b^unspecified flies show a small but significant ventromedial shift of Mmus\Cd8a^Mz19-positive projection neuron dendrite targeting. There is an additional significant ventromedial shift for these dendrites if the flies are also expressing Sema-2a^GD5476 under the control of Scer\GAL4^peb-GAL4.

In Sema-2a⁰³⁴⁷⁴ Sema-2b^unspecified double mutant projection neuron anterodorsal neuroblast clones generated between 0-24 hours after larval hatching (ALH), VM2 projection neuron dendrites mistarget dorsolaterally. In contrast, if the double mutant clones are generated between 48-72 hours ALH, VM2 dendrites target normally to the ventromedial VM2 glomerulus.

(Sweeney et al., 2011)

In stage 14-16 Sema-2a⁰³⁴⁷⁴/+;; Df(4)C3/+ embryos, v'ch1 axon mis-projections to the intersegmental nerve are found in 3.7% of hemisegments, and 1ch5 mis-projections to the segmental nerve are found in 4.9% of hemisegments, which is significantly higher than that seen in either Sema-2a⁰³⁴⁷⁴ or Df(4)C3 heterozygotes alone.

Transheterozygous Sema-2a⁰³⁴⁷⁴/+;; PlexB^KG00878 embryos exhibit v'ch1 mis-projections to the intersegmental nerve (4.4%) and lateral axon mis-projections to the segmental nerve or stalls (2.4%), at frequencies significantly higher than in Sema-2a⁰³⁴⁷⁴ or PlexB^KG00878 heterozygotes.

(Bates and Whitington, 2007)

Removing one or both copies of Sema-2a gives dosage-sensitive suppression of the Netrin-mediated RP3 phenotype of Ts(1Lt;YSt)B118+Ts(1Rt;YLt)T9 mutants. Scer\GAL4^how-24B-mediated expression of NetB^Scer\UAS.cHa causes the SNc to extend for only a short distance, ending in a clump. When the SN reaches the lateral muscle domain the SNa often fails to branch. Loss of Sema-2a expression allows both the SNa and SNc to project normally.

(Winberg et al., 1998)

Xenogenetic Interactions

Statement

Reference

Complementation and Rescue Data

Fails to complement

Sema2a⁰³⁰²¹

(BDGP Project Members, 1994-1999)

Rescued by

Sema2a⁰³⁴⁷⁴ is rescued by Sema2a^UAS.cKa/Scer\GAL4^salm-459.2

(Bates and Whitington, 2007)

Comments

Expression of Sema-2a^Scer\UAS.cKa under the control of Scer\GAL4^peb-GAL4 is sufficient to rescue the ventromedial targeting defects of Mmus\Cd8a^Mz19-positive projection neuron dendrites seen in Sema-2a⁰³⁴⁷⁴ Sema-2b^unspecified double homozygous flies.

(Sweeney et al., 2011)

Images (0)

Mutant

Wild-type

Stocks (0)

Notes on Origin

Discoverer

A. Spradling.

Comments

Dysgenesis-induced loss of the P element can revert the phenotype to wild type.

(Kolodkin et al., 1993)

External Crossreferences and Linkouts ( 0 )

Synonyms and Secondary IDs (9)

Reported As

Symbol Synonym

Sema-2a⁰³⁴⁷⁴

Sema2a⁰³⁴⁷⁴

(BDGP Project Members, 1994-1999)

SemaII^P2

(Winberg et al., 1998)

l(2)03474

l(2)Sema-2a³⁴⁷⁴

(Hanlon and Andrew, 2016)

sema-2a^P2

(Meltzer et al., 2016, Sweeney et al., 2011)

sema-II⁰³⁴⁷⁴

sema2a⁰³⁴⁷⁴

(Bates and Whitington, 2007)

semaII^P2

(Bates and Whitington, 2007, Kolodkin et al., 1993)

Name Synonyms

Secondary FlyBase IDs

References (9)

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