Max-Planck-Institut für biologische Kybernetik, Tübingen, F.R.G.,
The involvement of the protocerebral bridge (pb) in the control of step length was initially suggested by corresponding impairments found in the mutant no-bridgeKS49 (nob) and its mosaics (Strauss et al. 1992, J Neurogenet 8:125-155). The mutant invariably has a median gap in the pb, a rod-shaped neuropil belonging to the central complex of the protocerebrum of all insects. The steps of nobKS49 flies are consistently short, regardless of the actual stepping frequency, whereas in wildtype (WT) flies step length increases with increasing stepping frequency.
Recently, the pb of ocelliless1 (oc1) mutant flies was also reported to be severely disrupted (Hirth et al. 1995, Neuron 15:769-778). Most of the pb is missing and only the outermost glomeruli exist. Only in some individuals were we able to find small remainders of neuropil which are likely to be part of the pb material.
In all of the walking paradigms tested oc1 flies walk significantly slower than WT flies. Further analysis with our automated walking detector (Strauss 1993, J Neurogenet 8:250) revealed that step lengths are markedly less dependent on stepping frequency than in WT flies. At low stepping frequencies the step lengths of oc1 and WT flies are indistinguishable from one another, whereas at high stepping frequencies they become markedly different. Our ongoing mosaic analysis shows full correlation with the state of the pb. In contrast to other pb-defective mutant strains oc1 has practically no reduction in walking activity.
The role of the pb in stepping is further elucidated by our new mutant line C141 isolated in a behavioral screen for walking impaired X-linked mutants (Strauss, J Neurogenet, in press). Its pb-defect is less prominent than in nobKS49 and oc1, and comprises a constriction or even an interruption at the sagittal midplane. In these flies the step length is almost independent of the stepping frequency, whereas the absolute step length is less affected.
The reductions in step length were found in mutants of three independent genes with gross anatomical lesions in the pb. The finding strongly supports the notion that the pb is indeed involved in the adjustment of step length in order to optimize walking speed.