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Lamina-medulla Connections in Structural Brain Mutants |
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While several phases of eye development can already be described in detailled cellular and even molecular terms, understanding of optic lobe development is lagging behind (see e.g. respective reviews in Bate and Martinez Arias, 1993). This is partially due to its 3-dimensional complexity, to the much larger number of cell types involved, and to the fact that the selection of mutant phenotypes of the optic lobe requires dissection. The latter hindered easy access to specific mutants. In contrast, a huge number of eye mutations has accumulated. Due to them it is at least known that optic lobe development depends strongly on the normal ingrowth of retinula axons (Power, 1943; Meyerowitz and Kankel, 1978; Garen and Kankel, 1983; Selleck and Steller, 1991; Selleck et al., 1992). The first mutant screen not neglecting structural optic lobe-specific phenotypes was that performed by Heisenberg and Böhl (1979). Some of the isolated EMS-induced mutants - like alleles of small optic lobes - were indeed shown to act autonomously on the optic lobe (Fischbach and Technau, 1984). Other mutants - like the first, P-element induced irreC allel, which was isolated in another screen for structural brain mutants (Fischbach et al., 1987), showed independent foci in the compound eye and optic lobe (Boschert et al., 1990).
This poster describes some important facets of the small optic lobes and irreC phenotypes by use of the Golgi method. Emphasis is on the columnar neurons that connect retina and lamina with the medulla.
The Golgi impregnations were carried out following the procedure of Colonnier (1964), slightly adjusted as described in Fischbach and Dittrich (1989). Specimen were embedded in Araldite and 35 µm section were taken.
Camera lucida drawings of single neurons were done and the relative position of cells in the optic lobe recorded. Individual drawings were then used to compose the Figures shown in this poster.
Results: Golgi shapes of columnar neurons connecting lamina and medulla in structural mutants
Discussion
small optic lobes (KS58) : Genetic mosaic analysis has shown that the genotype of the medulla cortex is responsible for the mutant phenotype (small optic lobes resulting from cell degeneration in the pupal stage; Fischbach and Technau (1984)). It has also been shown that the volume of the lamina is about normal in sol mutants (Fischbach et al., 1989) and by antibody staining that at least the T1 neurons do occur in normal number (one in each column). The Golgi data presented here show that the neuronal shapes are fairly normal at the level of the lamina, while they are clearly aberrant at the level of the medulla. The altered (enlarged) arborizations of projections into the medulla may reflect their response to the absence of about 50% of all columnar medulla neurons.
irregular chiasm C (UB883) : The irregular chiasm C (UB883) mutation is a P-element insertion in 3C5 into the 5'-region of the irreC-rst gene partially suppressing its transcription. The gene codes for a new member of the immunoglobulin superfamily (Ramos et al., 1993). The molecular function of this protein in axonal pathfinding (Schneider et al., 1995) and eye development (Reiter et al., submitted) is presently under investigation. Here we want to point to the fact that the misprojecting fibers exiting the posterior lamina terminate in about the right retinotopic region of the anterior medulla. Therefore irreC -mutants might be well suited to screen for genes involved in target recognition.
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