FB2025_04 , released October 2, 2025
Allele: Dmel\Sema2a03021
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General Information
Symbol
Dmel\Sema2a03021
Species
D. melanogaster
Name
FlyBase ID
FBal0015411
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Also Known As
SemaIIP1, l(2)03021, P{PZ}Sema-2a03021
Key Links
Genomic Maps

Nature of the Allele
Progenitor genotype
Associated Insertion(s)
Cytology
Description

P-element insert at codon 33 of the open reading frame.

P element inserted in the middle of the codon for amino acid 32 in the open reading frame.

Allele components
Component
Use(s)
Inserted element
Encoded product / tool
Mutations Mapped to the Genome
Associated Sequence Data
DNA sequence
Protein sequence
 
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

abdominal lateral oblique muscle 1 & neuromuscular junction

abdominal segment border muscle & neuromuscular junction

abdominal ventral longitudinal muscle 2 & neuromuscular junction

abdominal ventral longitudinal muscle 3 & neuromuscular junction

abdominal ventral longitudinal muscle 4 & neuromuscular junction

Detailed Description
Statement
Reference

Sema-2a03021/Df(2R)B65 mutant larvae do not display any increase in dendritic non-contacting crossing in the class IV dendritic arborizing neurons.

Approximately 9.7% 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. A second, less frequent defect is observed whereby one or more axons of the lateral cluster sensory neurons misproject ventrally, joining the v'ch1 axon and the segmental nerve, instead of the intersegmental 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.

Sema-2a03021 homozygous mutant embryos exhibit normal projection of the ISN and SN axons in all hemisegments in which v'ch1 and dorsal sensory axon defects occur.

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.

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.

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
Enhanced by
Statement
Reference
NOT Enhanced by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference
Phenotype Manifest In
Enhanced by
Statement
Reference
NOT Enhanced by
Statement
Reference
NOT suppressed by
Statement
Reference
Enhancer of
Statement
Reference

Sema2a03021 is an enhancer of eye phenotype of KrIf-1

Sema2a03021 is an enhancer of ommatidium phenotype of KrIf-1

Additional Comments
Genetic Interactions
Statement
Reference

Sema-1ak13702 Sema-2a03021 double mutants exhibit sensory axon mis-projections in the same frequency as Sema-2a03021 homozygotes.

Sema-2a03021;;Df(4)C3 double mutant embryos show v'ch1 mis-projections (24.5% of hemisegments) and lateral axon mis-projections (7.5% of hemisegments) at higher penetrance levels than are seen in either single homozygous mutant.

Sema-2a03021;;PlexBKG00878 double homozygotes show v'ch1 mis-projections (27.8% of hemisegments) and lateral axon mis-projections (4.2% of hemisegments) at higher levels than in either single homozygous mutant.

Sema-2a03021/+; SoxNGA1192/+ mutants are viable.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

A. Spradling.

Comments
Comments

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

Complements: Cdk405428. Complements: Hmgs06214. Complements: l(2)k07127k07127. Complements: l(2)k07824k07824. Complements: l(2)k07824k07828. Complements: Ca-P60Ak08308ab. Complements: vegk17010. Complements: scbk17029a. Complements: Cdk4s4639.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (9)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (12)