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).