Chapter 14 : The Role of Bacterial Channels in Cell Physiology

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This chapter provides an overview on the role of bacterial channels in cell physiology. The proposed role of mechanosensitive (MS) channels is the rapid and nonspecific release of solutes from the cell in response to the generation of excessive turgor pressure. This model has now been tested and verified for . In most bacterial cells Cl ions have not been predicted to have significant roles in cell physiology. In some halophilic bacteria Cl is accumulated to provide salt balance during growth in very high salt concentrations. The aquaglyceroporins are pores that allow the permeation of water and small linear polyhydric molecules through the bacterial membrane. The cell faces two types of problems that relate to ammonium ions. First, there is the need to scavenge for ammonium when the concentration in the environment is low. Second, cells growing on broth may encounter a surfeit of cytoplasmic ammonium ions arising from the deamination of amino acids. In a wide range of bacterial genera the genes for AmtB and GlnK exist as an operon, and recent work suggests that the former is a pore that is used by cells to accelerate the passage of ammonium ions across the membrane and that GlnK is a specific component of the nitrogen-regulatory circuit that controls its activity. The increased understanding of mechanistic aspects of the channel selectivity and gating has advanced rapidly, but an appreciation of the role of channels in cell physiology lags well behind.

Citation: Booth I, Edwards M, Murray E, Miller S. 2005. The Role of Bacterial Channels in Cell Physiology, p 291-312. In Kubalski A, Martinac B (ed), Bacterial Ion Channels and Their Eukaryotic Homologs. ASM Press, Washington, DC. doi: 10.1128/9781555816452.ch14
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Image of Figure 1.
Figure 1.

Consequences of channel gating for bacterial cells. The figure depicts the consequences of ion channel gating for a K-specific channel (left) and an MS channel (right). The internal and external ion concentrations depicted are based on published values (see text for detail), and the changes in membrane potential, ion concentrations, and cytoplasmic pH value are based on previously published calculations that use data for the capacitance of the cytoplasmic membrane (see text) ( ). Initially the cell is depicted with the channels closed (a) with typical cell and environmental concentrations of inorganic ions (note that bacterial cells will also contain ∼60 to 150 mM glutamate as the major osmotically active anion, plus lower concentrations of acetate and other organic anions [ ]). Upon gating the channels for 1 ms (b) or 1 s (c), there are major changes in ion pools when MS channels fire, but much less so for K channels, with the consequence that the latter, but not the former, can be used to generate a membrane potential. Note that unless there is a substantial inward leak current, a voltage-gated K channel would be unlikely to sustain the open state for 1 s, whereas a ligand-gated channel could remain open as long as the ligand remains bound. For an MS channel an open state of 1 s is frequently seen in patch-clamp recordings but is not considered physiologically relevant during hypoosmotic shock when channel activation would dissipate the pressure differential required for channel activation in milliseconds.

Citation: Booth I, Edwards M, Murray E, Miller S. 2005. The Role of Bacterial Channels in Cell Physiology, p 291-312. In Kubalski A, Martinac B (ed), Bacterial Ion Channels and Their Eukaryotic Homologs. ASM Press, Washington, DC. doi: 10.1128/9781555816452.ch14
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Image of Figure 2.
Figure 2.

Ligand gating of bacterial channels. The figure illustrates the different types of K and Na channels (and pore) now known to be located in bacterial and archaeal cells. The majority of these possess the classical P-type structure, but there is another class, of which KefC is currently the best example, of gated systems. The nature of the ligand and the site of its action (periplasm, cytoplasm or membrane) are indicated. Further details on these channels are provided elsewhere ( ). ΔΦ, membrane potential; GSX, glutathione adducts; X, polyamines; Glut, glutamate.

Citation: Booth I, Edwards M, Murray E, Miller S. 2005. The Role of Bacterial Channels in Cell Physiology, p 291-312. In Kubalski A, Martinac B (ed), Bacterial Ion Channels and Their Eukaryotic Homologs. ASM Press, Washington, DC. doi: 10.1128/9781555816452.ch14
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Image of Figure 3.
Figure 3.

The consequences of electrophile activation of KefC. The formation of an adduct between MG and GSH provides the substrate, hemithiolacetal (HTA), for glyoxalase I (GlyI). The product of GlyI action is SLG, which is the primary activator of KefB and KefC. Further detoxification is undertaken by glyoxalase II (GlyII), regenerating GSH and forming D-lactate. GSH and SLG are negative and positive regulators, respectively, of KefB and KefC. The result is K efflux from the cell, and this is accompanied by H and Na entry by a route not yet identified. It has been demonstrated that the acidification of the cytoplasm aids cell survival of cells ( ), protecting the DNA against damage by MG ( ).

Citation: Booth I, Edwards M, Murray E, Miller S. 2005. The Role of Bacterial Channels in Cell Physiology, p 291-312. In Kubalski A, Martinac B (ed), Bacterial Ion Channels and Their Eukaryotic Homologs. ASM Press, Washington, DC. doi: 10.1128/9781555816452.ch14
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Table 1.

Types of bacterial and archaeal ion channels

Citation: Booth I, Edwards M, Murray E, Miller S. 2005. The Role of Bacterial Channels in Cell Physiology, p 291-312. In Kubalski A, Martinac B (ed), Bacterial Ion Channels and Their Eukaryotic Homologs. ASM Press, Washington, DC. doi: 10.1128/9781555816452.ch14

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