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General Information
Symbol
Dmel\slgA1
Species
D. melanogaster
Name
FlyBase ID
FBal0015697
Feature type
allele
Associated gene
Associated Insertion(s)
Carried in Construct
Key Links
Nature of the Allele
Mutations Mapped to the Genome
 
Type
Location
Additional Notes
References
Associated Sequence Data
DNA sequence
Protein sequence
 
 
Progenitor genotype
Cytology
Nature of the lesion
Statement
Reference

No polymorphism detectable with Southern blot.

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
Detailed Description
Statement
Reference

Mosaic analysis indicates that the focus of the slgA mutation maps to the thoracic ganglion. Proline oxidase levels are dramatically reduced, and free proline elevated in mutants.

Homozygous viable. Homozygous germline clones display no maternal effect. Flies derived from heterozygous mothers do not move towards a light source.

slgA1/Df(1)Q539 flies have reduced viability and show defective phototaxis. slgA1/Df(1)GA104 flies have reduced viability, defective phototaxis, severe motor debilitation and are often mired in the food medium. They also have a weak or non-existent optomotor response. slgA1/Df(1)GE263 flies have reduced viability, defective phototaxis, show uncoordinated behaviour and have a weak or non-existent optomotor response. slgA1/Df(1)17-257 flies have reduced viability, defective phototaxis and a weak or non-existent optomotor response.

slgA1 flies do not have small optic lobes.

Isolated as defective in fast phototaxis, using counter-current-distribution (CCD) machine; also turned out to have poor (negative) geotaxis in this machine; yet mutant males showed some positive optomotor responses and had a normal electroretinogram; hence termed sluggish (as opposed to phototaxis-defective per se); Markow and Merriam (1977) confirmed aberrant CCD phototactic response; in maze tests the mutant was found to be quite photonegative (more so than wild type) and seemingly normal in geotaxis (Markow and Merriam, 1977). slgA causes poor viability, as well as aberrant behavior in hemizygous females (Miklos et al., 1987); in mosaics studied for sluggishness, a mutant leg seemed to be debilitated independently of behavior of other legs, with the six foci for such movement deficits mapping to the ventral blastoderm (A. Ghysen, cited in Hall, 1978).

External Data
Interactions
Show genetic interaction network for Enhancers & Suppressors
Phenotypic Class
NOT suppressed by
Statement
Reference

slgA1 has abnormal phototaxis phenotype, non-suppressible by Septin1GL1

Phenotype Manifest In
Additional Comments
Genetic Interactions
Statement
Reference

Mutant phototactic behaviour and inactivity phenotypes of slgA1 are not rescued by Sep1GL1. Proline oxidase levels are dramatically reduced, and free proline elevated in mutants, and these effects are also not rescued by Sep1GL1.

Xenogenetic Interactions
Statement
Reference
Complementation and Rescue Data
Rescued by
Comments

Mutant phototactic behaviour and inactivity phenotypes of slgA1 rescued by slgA+t14.7. Proline oxidase levels are dramatically reduced, and free proline elevated in mutants, and these effects are also rescued by slgA+t14.7.

Images (0)
Mutant
Wild-type
Stocks (1)
Notes on Origin
Discoverer

Eichenberger and Benzer.

Comments
Comments

slgA1 is not an allele of sol; slgA1 complements the mutations sol9, sol3, sol4, sol6 and sol1 with regard to photo- and geotaxis.

External Crossreferences and Linkouts ( 0 )
Synonyms and Secondary IDs (3)
Reported As
Name Synonyms
Secondary FlyBase IDs
    References (5)