Der Rüsselkäfer Chlorophanus viridis reagiert wie viele andere Organismen auf Bewegungen in seiner optischen Umwelt mit charakteristischen Verhaltensweisen. Dem liegt eine Auswertung von Relationen zwischen einzelnen Lichtreizen zugrunde. Die Funktionsstruktur dieser Auswertungsleistung wird ermittelt. Das Ergebnis der Analyse ist in Abb. 8 dargestellt.

An understanding of sensory information processing in the nervous system will probably require investigations with a variety of ‘model’ systems at different levels of complexity.Our choice of a suitable model system was constrained by two conflicting requirements: on one hand the information processing properties of the system should be rather complex, on the other hand the system should be amenable to a quantitative analysis. In this sense the fly represents a compromise.In these two papers we explore how optical information is processed by the fly's visual system. Our objective is to unravel the logical organization of the fly's visual system and its underlying functional and computational principles. Our approach is at a highly integrative level. There are different levels of analysing and ‘understanding’ complex systems, like a brain or a sophisticated computer.

The paper is dealing in its first part with a system-theoretical approach for the decomposition of multi-input systems into the sum of simpler systems. By this approach the algorithm for the computations underlying the extraction of motion information from the optical environment by biological movement detectors is analysed. In the second part it concentrates on a specific model for motion computation known to be realized by the visual system of insects and of man. These motion detectors provide the visual system with information on both, velocity and structural properties of a moving pattern. The last part of the paper deals with the functional properties of two-dimensional arrays of movement detectors. They are analyzed and their relations to meaningful physiological responses are discussed.

Cysteine proteases have been implicated as important virulence factors in a wide range of prokaryotic and eukaryotic pathogens, but little direct evidence has been presented to support this notion. Virtually all strains of the human bacterial pathogen Streptococcus pyogenes express a highly conserved extracellular cysteine protease known as streptococcal pyrogenic exotoxin B (SpeB). Two sets of isogenic strains deficient in SpeB cysteine protease activity were constructed by integrational mutagenesis using nonreplicating recombinant plasmids containing a truncated segment of the speB gene. Immunoblot analyses and enzyme assays confirmed that the mutant derivatives were deficient in expression of enzymatically active SpeB cysteine protease. To test the hypothesis that the cysteine protease participates in host mortality, we assessed the ability of serotype M3 and M49 wild-type strains and isogenic protease-negative mutants to cause death in outbred mice after intraperitoneal inoculation. Compared to wild-type parental organisms, the serotype M3 speB mutant lost virtually all ability to cause mouse death ( P Ͻ 0.00001), and similarly, the virulence of the M49 mutant was detrimentally altered ( P Ͻ 0.005). The data unambiguously demonstrate that the streptococcal enzyme is a virulence factor, and thereby provide additional evidence that microbial cysteine proteases are critical in host-pathogen interactions.