Bacterial Stress Responses: What Doesn't Kill Them Can Make Them Stronger
نویسنده
چکیده
A n organism's survival from moment to moment depends, at least in part, on its ability to sense and respond to changes in its environment. Mechanisms for responding to environmental changes are universally present in living beings. For example, when mammals perceive a sudden environmental change as threatening, a rush of adrenaline precipitates the well-known " fi ght or fl ight " response. Such physiological stress responses in complex organisms require appropriately regulated interactions among numerous organ systems. But how do single-celled organisms respond to potentially lethal threats? The hope is that identifying specifi c mechanisms that contribute to microbial survival under rapidly changing conditions will provide insight into stress response systems across life forms. Bacteria—and especially those capable of persisting in diverse environments, such as Escherichia coli—provide particularly valuable models for exploring how single-celled organisms respond to environmental stresses. For example, most bacteria associated with foodborne infections (e.g., some E. coli serotypes, Salmonella enterica serovar Typhimurium, Listeria monocytogenes) can survive under diverse conditions, both inside and outside of the host. To ultimately cause human infection, a foodborne pathogen must fi rst survive transit in food or water, a signifi cant achievement since the majority of commercial products destined for consumption in the United States are treated with strategies specifi cally designed to control or eliminate microbial contaminants. Following ingestion, the bacterium must survive exposure to conditions that have evolved to provide the host with some protection against pathogenic microbes. Human bodily defenses include gastric acid (ranging from [pH 2.5–4.5], largely depending on feeding status), bile salts, and organic acids within the gastrointestinal tract. To survive these extreme and rapidly changing conditions, bacteria must sense the changes and then respond with appropriate alterations in gene expression and protein activity. Therefore, one important scientifi c challenge is to identify mechanisms that control the switch or switches that allow free-living bacteria to adjust to and invade a host organism. In bacteria, alterations in gene expression are often controlled at the transcriptional level through changes in associations between the catalytic core of RNA polymerase and the different sigma factors present in a bacterial cell [1]. RNA polymerase is the enzyme responsible for recognizing appropriate genes under specifi c environmental conditions, and for creating the mRNA transcripts that can be translated into new proteins. Sigma factors are dissociable subunits of prokaryotic RNA polymerase. When a sigma factor associates with a core RNA polymerase to …
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ورودعنوان ژورنال:
- PLoS Biology
دوره 4 شماره
صفحات -
تاریخ انتشار 2006