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Alterations to aquatic environments, via natural or anthropogenic factors can directly or indirectly lead to infectious disease outbreaks. At present, little information is available on the molecular ecology and evolutionary dynamics of infectious agents in the environment. Understanding the environmental factors involved in persistence, growth, and transmission of pathogens, as well as the response of organisms to environmental changes, will provide information about the emergence or re-emergence of infectious diseases. V. cholerae is an excellent model system to study these processes, because it causes periodic, seasonal outbreaks of the disease in regions where it is an established member of the indigenous aquatic flora. It is estimated that the disease causes the death of 120,000 people worldwide every year. V. cholerae's capacity to cause seasonal epidemics is linked to its survival in free-living and in biofilm growth modes in aquatic environments between outbreaks. However, the processes governing the survival of V. cholerae and its adaptability to changes in habitat remain elusive.
V. cholerae has two phase variants, called smooth and rugose, reflecting the appearance of their colonial morphologies. Reversible phase variation between the rugose and the smooth colonial variants and associated phenotypes is postulated to be an important factor for the survival of the organism. Little is known about the molecular basis of the phase variation or molecular differences between these two colonial variants. Using molecular genetic and genomic approaches, Yildiz's laboratory is attempting to identify and characterize the genes and processes associated with the phase variation. In aquatic habitats, V. cholerae is found attached to various biotic and abiotic surfaces. It has been proposed that attachment of bacteria to surfaces and the subsequent biofilm growth mode exemplify a survival strategy. Identification of the genes required for the development of V. cholerae biofilms, as well as the metabolic pathways operating in these biofilms, is central to understanding the sessile lifecycle of the organism. At present, very little is known about the processes that allow V. cholerae to sense, respond, and adapt to life on a surface. Yildiz' research group combines molecular genetics, functional genomics, proteomics, microbial ecology and microscopy to investigate the signals and regulatory networks that are essential for V. cholerae biofilm formation. Results obtained through their research projects will expand our understanding of the environmental life cycle of an important human pathogen and will provide information useful for the prediction and control of cholera epidemics.
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