Furthermore, extensive research around the physiology, cell biology, and immunology of the mammalian host provides an excellent opportunity to probe the functional significance of cell shape, as each of these host features likely exerts selective pressures on bacteria that transiently or chronically colonize humans to cause disease. the selective pressures that drive the diverse forms (or cell wall compositions) observed in mammalian pathogens and bacteria more generally, including efficient adherence to biotic and abiotic surfaces, survival under low-nutrient or nerve-racking conditions, evasion of mammalian match deposition, efficient dispersal through mucous barriers and tissues, and efficient nutrient acquisition. INTRODUCTION Van Leeuwenhoek’s microscopes opened our eyes to the microbial world and its large quantity of forms. Bacteria were in the beginning characterized on the basis of morphology, but over time, phylogenetics has proven to be a more UNC0321 strong method for classifying bacteria. In the medical center, biochemical characteristics (recently including those observed by mass spectrometry) and growth on various indication media robustly distinguish bacterial pathogens, and thus there is little incentive to directly observe bacteria. Even in the research lab, cell biology methods often focus on morphological changes to the host cell during contamination, not the morphology of the pathogen itself. Still, both pathogenic and nonpathogenic bacteria show considerable morphological diversity. In this review, we consider the functional consequences of differences in form on bacterial survival in native environments (as opposed to culture flasks of rich media). The work reviewed here builds on pioneering studies and hypotheses explained in several excellent reviews around the possible selective effects of bacterial cell shape diversity (1,C5). We explore several aspects of morphological diversity (Table 1). Bacteria have unique cell body designs, ranging from spheres (cocci) to rods (bacilli) of various curvatures and helicities and to more exotic shapes, such as stars, created by elaboration of prosthecae through polar growth. Bacteria can also produce a variety of appendages, such as pili or flagella, which show diversity in overall shape, length, and width as well as placement with respect to the cell body. Finally, bacteria can change morphology during their life cycle or in response to UNC0321 environmental conditions. Much of our understanding of the mechanisms that produce different shapes comes from the study of model organisms under laboratory growth conditions. Increasingly, experts studying pathogenic bacteria in the context of infection models have observed morphological diversity and/or observed that mutants with altered colonization or virulence properties have an altered shape. This has led to speculation that cell shape itself may be a virulence factor or that this mammalian host environment(s) imposes a selective pressure driving morphological diversity. In some cases, studies of shape in model organisms under conditions mimicking natural environments have revealed selective causes that likely are relevant to pathogenic lifestyles. This field has made significant progress recently in part due to improvements in imaging that allow interrogation of individual bacterial cells on multiple time scales and resolution of bacterial subcellular structures. While this review focuses mostly on recent work on pathogens, we also spotlight work on nonpathogenic organisms that illuminates functional principles UNC0321 and methodologies that will likely translate to the study of pathogens. Rabbit Polyclonal to OPRK1 TABLE 1 Examples of bacterial morphological variance and functional effects(coccoid) and (ovococcoid) as well as the Gram-negative coccoid pathogens and and have been analyzed in great depth by numerous groups over the years, and much of our understanding of bacterial processes in cocci has come from this body of work. Studies looking at PG synthesis in both coccoid and ovococcoid bacteria have helped to inform our understanding of how these basic shapes can be generated. It has been proposed that at least two different PG machineries exist to UNC0321 generate the ovococcoid shape, whereas only one PG synthesis complex is required to form a coccoid cell. Coccoid bacteria, such as and other ovococcoid bacteria synthesize new cell walls by using both the cell division machinery (septal PG) and an elongation complex (peripheral PG) (21, 22). Incomplete or delayed cell division of ovococci results in chains or filaments, as these cells divide in one plane perpendicular to the long axis of the cell. Coccoid cells, however, alternate their division axes along two or three planes, which can.