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Fig. 8. The -spectrin gene is affected in klötzchen mutants. (A-F) CNS preparations of stage-16 embryos stained for BP102 (A-D) or ß-Spectrin (E,F). (A) Wild-type embryos are characterized by a regular axonal pattern with separated segmental commissures and longitudinal connectives. (B) Homozygous E2-26-mutant embryos show partially fused commissures. (C) A homozygous E2-26 mutant with no further background mutations shows no axonal phenotype. (D) When such embryos are allowed to develop at 4°C for 1 day, a fused-commissure phenotype develops. (E) ß-Spectrin protein in the ventral nerve cord of wild-type embryos. (F) In homozygous E2-26 mutants, ß-Spectrin expression in the neuropil appears altered. (G) -Spectrin protein expression in some of the -spectrin mutants. Proteins were isolated from ten stage 16/17 embryos and were separated on a 6% SDS gel. Following western blotting, -Spectrin expression was detected using the monoclonal antibody 3A9. w¹¹¹⁸ embryos were used as a wild-type control. If not otherwise indicated, homozygous mutants were used. Genotypes are as indicated. The P-2 mutation does not lead to a detectable truncation of -Spectrin. In N-2 and, possibly, 1.3 mutants, a slight reduction of the -Spectrin protein size is noted. In the deficiency Aprt32, and in the mutants rg41 and E2-26 all zygotic -Spectrin expression is removed. Only maternal -Spectrin expression is visible. (H) To control for equal loading, the same membrane was probed with anti-Kette antibodies.

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