Errors that alter the reading frame occur extremely rarely during translation, yet some genes have evolved sequences that efficiently induce frameshifting. These sequences, termed programmed frameshift sites, manipulate the translational apparatus to promote non-canonical decoding. Frameshifts are mechanistically diverse. Most cause a -1 shift of frames; the first such site was discovered in a metazoan retrovirus, but they are now known to be dispersed quite widely among evolutionarily diverse species. +1 frameshift sites are much less common, but again dispersed widely. The rarest form are the translational hop sites which program the ribosome to bypass a region of several dozen nucleotides. Each of these types of events are stimulated by distinct mechanisms. All of the events share a common phenomenology in which the programmed frameshift site causes the ribosome to pause during elongation so that the kinetically unfavorable alternative decoding event can occur. During this pause most frameshifts occur because one or more ribosome-bound tRNAs slip between cognate or near-cognate codons. However, even this generalization is not entirely consistent, since some frameshifts occur without slippage. Because of their similarity to rarer translational errors, programmed frameshift sites provide a tool with which to probe the mechanism of frame maintenance.
Our review of the metabolic pathways of pyridines and aza-arenes showed that biodegradation of heterocyclic aromatic compounds occurs under both aerobic and anaerobic conditions. Depending upon the environmental conditions, different types of bacteria, fungi, and enzymes are involved in the degradation process of these compounds. Our review indicated that different organisms are using different pathways to biotransform a substrate. Our review also showed that the transformation rate of the pyridine derivatives is dependent on the substituents. For example, pyridine carboxylic acids have the highest transformation rate followed by mono-hydroxypyridines, methylpyridines, aminopyridines, and halogenated pyridines. Through the isolation of metabolites, it was possible to demonstrate the mineralization pathway of various heterocyclic aromatic compounds. By using 14C-labeled substrates, it was possible to show that ring fission of a specific heterocyclic compound occurs at a specific position of the ring. Furthermore, many researchers have been able to isolate and characterize the microorganisms or even the enzymes involved in the transformation of these compounds or their derivatives. In studies involving 18O labeling as well as the use of cofactors and coenzymes, it was possible to prove that specific enzymes (e.g., mono- or dioxygenases) are involved in a particular degradation step. By using H2 18O, it could be shown that in certain transformation reactions, the oxygen was derived from water and that therefore these reactions might also occur under anaerobic conditions.
The most fundamental questions such as whether a cell is alive, in the sense of being able to divide or to form a colony, may sometimes be very hard to answer, since even axenic microbial cultures are extremely heterogeneous. Analyses that seek to correlate such things as viability, which is a property of an individual cell, with macroscopic measurements of culture variables such as ATP content, respiratory activity, and so on, must inevitably fail. It is therefore necessary to make physiological measurements on individual cells. Flow cytometry is such a technique, which allows one to analyze cells rapidly and individually and permits the quantitative analysis of microbial heterogeneity. It therefore offers many advantages over conventional measurements for both routine and more exploratory analyses of microbial properties. While the technique has been widely applied to the study of mammalian cells, is use in microbiology has until recently been much more limited, largely because of the smaller size of microbes and the consequently smaller optical signals obtainable from them. Since these technical barriers no longer hold, flow cytometry with appropriate stains has been used for the rapid discrimination and identification of microbial cells, for the rapid assessment of viability and of the heterogeneous distributions of a wealth of other more detailed physiological properties, for the analysis of antimicrobial drug-cell interactions, and for the isolation of high-yielding strains of biotechnological interest. Flow cytometric analyses provide an abundance of multivariate data, and special methods have been devised to exploit these. Ongoing advances mean that modern flow cytometers may now be used by nonspecialists to effect a renaissance in our understanding of microbial heterogeneity.
Methane-utilizing bacteria (methanotrophs) are a diverse group of gram-negative bacteria that are related to other members of the Proteobacteria. These bacteria are classified into three groups based on the pathways used for assimilation of formaldehyde, the major source of cell carbon, and other physiological and morphological features. The type I and type X methanotrophs are found within the gamma subdivision of the Proteobacteria and employ the ribulose monophosphate pathway for formaldehyde assimilation, whereas type II methanotrophs, which employ the serine pathway for formaldehyde assimilation, form a coherent cluster within the beta subdivision of the Proteobacteria. Methanotrophic bacteria are ubiquitous. The growth of type II bacteria appears to be favored in environments that contain relatively high levels of methane, low levels of dissolved oxygen, and limiting concentrations of combined nitrogen and/or copper. Type I methanotrophs appear to be dominant in environments in which methane is limiting and combined nitrogen and copper levels are relatively high. These bacteria serve as biofilters for the oxidation of methane produced in anaerobic environments, and when oxygen is present in soils, atmospheric methane is oxidized. Their activities in nature are greatly influenced by agricultural practices and other human activities. Recent evidence indicates that naturally occurring, uncultured methanotrophs represent new genera. Methanotrophs that are capable of oxidizing methane at atmospheric levels exhibit methane oxidation kinetics different from those of methanotrophs available in pure cultures. A limited number of methanotrophs have the genetic capacity to synthesize a soluble methane monooxygenase which catalyzes the rapid oxidation of environmental pollutants including trichloroethylene.
INTRODUCTION ...........................................................................................................................................................1 GENETIC REGULATION.............................................................................................................................................2 Biosynthetic Pathways................................................................................................................................................2 Phosphatidic acid and CDP-diacylglycerol synthesis ........................................................................................2 Phosphatidylinositol branch..................................................................................................................................4 Phosphatidylcholine branch: de novo pathway...................................................................................................5 Phosphatidylcholine branch: salvage pathway....................................................................................................6 Inositol and choline transporters .........................................................................................................................6 Cardiolipin branch .................................................................................................................................................7 Sphingolipids ...........................................................................................................................................................8 Fatty acids................................................................................................................................................................8 Cross-Pathway Regulation.........................................................................................................................................8 Control by Factors Affecting Mitochondrial Development ...................................................................................9 LEVELS OF REGULATION.........................................................................................................................................9 INOSITOL/CHOLINE RESPONSE...........................................................................................................................10 UASINO Regulatory Sequence..................................................................................................................................10 INO2 and INO4 Positive Regulatory Genes ..........................................................................................................11 OPI1 Negative Regulatory Gene .............................................................................................................................12 Other Regulatory Genes ..........................................................................................................................................13 Autoregulation of INO2 Expression .......................................................................................................................13 URS1 Regulatory Sequence ..............................................................................................................................14 SIN3 and UME6 Global Negative Regulators .......................................................................................................14 INO1 TRANSCRIPTION AND THE GENERAL TRANSCRIPTION MACHINERY .........................................14 REGULATION OF PHOSPHOLIPID BIOSYNTHESIS IN OTHER FUNGI.....................................................15 Schizosaccharomyces pombe.......................................................................................................................................15 Candida albicans ........................................................................................................................................................15 Neurospora crassa ......................................................................................................................................................16 CONCLUSIONS ...........................................................................................................................................................16 ACKNOWLEDGMENTS .............................................................................................................................................16 REFERENCES ..............................................................................................................................................................16
Production and consumption processes in soils contribute to the global cycles of many trace gases (CH4, CO, OCS, H2, N2O, and NO) that are relevant for atmospheric chemistry and climate. Soil microbial processes contribute substantially to the budgets of atmospheric trace gases. The flux of trace gases between soil and atmosphere is usually the result of simultaneously operating production and consumption processes in soil: The relevant processes are not yet proven with absolute certainty, but the following are likely for trace gas consumption: H2 oxidation by abiontic soil enzymes; CO cooxidation by the ammonium monooxygenase of nitrifying bacteria; CH4 oxidation by unknown methanotrophic bacteria that utilize CH4 for growth; OCS hydrolysis by bacteria containing carbonic anhydrase; N2O reduction to N2 by denitrifying bacteria; NO consumption by either reduction to N2O in denitrifiers or oxidation to nitrate in heterotrophic bacteria. Wetland soils, in contrast to upland soils are generally anoxic and thus support the production of trace gases (H2, CO, CH4, N2O, and NO) by anaerobic bacteria such as fermenters, methanogens, acetogens, sulfate reducers, and denitrifiers. Methane is the dominant gaseous product of anaerobic degradation of organic matter and is released into the atmosphere, whereas the other trace gases are only intermediates, which are mostly cycled within the anoxic habitat. A significant percentage of the produced methane is oxidized by methanotrophic bacteria at anoxic-oxic interfaces such as the soil surface and the root surface of aquatic plants that serve as conduits for O2 transport into and CH4 transport out of the wetland soils. The dominant production processes in upland soils are different from those in wetland soils and include H2 production by biological N2 fixation, CO production by chemical decomposition of soil organic matter, and NO and N2O production by nitrification and denitrification. The processes responsible for CH4 production in upland soils are completely unclear, as are the OCS production processes in general. A problem for future research is the attribution of trace gas metabolic processes not only to functional groups of microorganisms but also to particular taxa. Thus, it is completely unclear how important microbial diversity is for the control of trace gas flux at the ecosystem level. However, different microbial communities may be part of the reason for differences in trace gas metabolism, e.g., effects of nitrogen fertilizers on CH4 uptake by soil; decrease of CH4 production with decreasing temperature; or different rates and modes of NO and N2O production in different soils and under different conditions.
The myxobacteria are gram-negative prokaryotes in the delta group of the Proteobacteria. They go through a complex developmental cycle that involves group behavior as well as rudimentary multicellularity. This review summarizes and evaluates the recent research on such areas as cell-cell signaling mediated by extracellular signals as well as by cellular appendages, social motility, rippling, tactic behavior, fruiting body and myxospore morphogenesis, retrons, developmental regulation, the role of light and carotenoids, phase variation, and antibiotic production. Although the myxobacteria are unequivocally prokaryotic, they manifest a number of properties more frequently found among the eukarya, such as serine-threonine kinases, calmodulin-like proteins, steroids, a phosphatidylinositol cycle, and reverse transcriptase. The myxobacteria may have been Nature's earliest experiment in multicellularity.
Respiratory infections with Pseudomonas aeruginosa and Burkholderia cepacia play a major role in the pathogenesis of cystic fibrosis (CF). This review summarizes the latest advances in understanding host-pathogen interactions in CF with an emphasis on the role and control of conversion to mucoidy in P. aeruginosa, a phenomenon epitomizing the adaptation of this opportunistic pathogen to the chronic chourse of infection in CF, and on the innate resistance to antibiotics of B. cepacia, person-to-person spread, and sometimes rapidly fatal disease caused by this organism. While understanding the mechanism of conversion to mucoidy in P. aeruginosa has progressed to the point where this phenomenon has evolved into a model system for studying bacterial stress response in microbial pathogenesis, the more recent challenge with B. cepacia, which has emerged as a potent bona fide CF pathogen, is discussed in the context of clinical issues, taxonomy, transmission, and potential modes of pathogenicity.
Superantigens are microbial agents that have a strong effect on the immune response of the host. Their initial target is the T lymphocyte, but a whole cascade of immunological reactions ensues. It is thought that the microbe engages the immune system of the host to its own advantage, to facilitate persistent infection and/or transmission. In this review, we discuss in detail the structure and function of the superantigen encoded by the murine mammary tumor virus, a B-type retrovirus which is the causative agent of mammary carcinoma. We will also outline what has more recently become known about superantigen activity associated with two human herpesviruses, cytomegalovirus and Epstein-Barr virus. It is likely that we have only uncovered the tip of the iceberg in our discovery of microbial superantigens, and we predict a flood of new information on this topic shortly.
Progress in our understanding of several biological processes promises to broaden the usefulness of Escherichia coli as a tool for gene expression. There is an expanding choice of tightly regulated prokaryotic promoters suitable for achieving high-level gene expression. New host strains facilitate the formation of disulfide bonds in the reducing environment of the cytoplasm and offer higher protein yields by minimizing proteolytic degradation. Insights into the process of protein translocation across the bacterial membranes may eventually make it possible to achieve robust secretion of specific proteins into the culture medium. Studies involving molecular chaperones have shown that in specific cases, chaperones can be very effective for improved protein folding, solubility, and membrane transport. Negative results derived from such studies are also instructive in formulating different strategies. The remarkable increase in the availability of fusion partners offers a wide range of tools for improved protein folding, solubility, protection from proteases, yield, and secretion into the culture medium, as well as for detection and purification of recombinant proteins. Codon usage is known to present a potential impediment to high-level gene expression in E. coli. Although we still do not understand all the rules governing this phenomenon, it is apparent that "rare" codons, depending on their frequency and context, can have an adverse effect on protein levels. Usually, this problem can be alleviated by modification of the relevant codons or by coexpression of the cognate tRNA genes. Finally, the elucidation of specific determinants of protein degradation, a plethora of protease-deficient host strains, and methods to stabilize proteins afford new strategies to minimize proteolytic susceptibility of recombinant proteins in E. coli.
Multidrug efflux systems display the ability to transport a variety of structurally unrelated drugs from a cell and consequently are capable of conferring resistance to a diverse range of chemotherapeutic agents. This review examines multidrug efflux systems which use the proton motive force to drive drug transport. These proteins are likely to operate as multidrug/proton antiporters and have been identified in both prokaryotes and eukaryotes. Such proton-dependent multidrug efflux proteins belong to three distinct families or superfamilies of transport proteins: the major facilitator superfamily (MFS), the small multidrug resistance (SMR) family, and the resistance/ nodulation/cell division (RND) family. The MFS consists of symporters, antiporters, and uniporters with either 12 or 14 transmembrane-spanning segments (TMS), and we show that within the MFS, three separate families include various multidrug/proton antiport proteins. The SMR family consists of proteins with four TMS, and the multidrug efflux proteins within this family are the smallest known secondary transporters. The RND family consists of 12-TMS transport proteins and includes a number of multidrug efflux proteins with particularly broad substrate specificity. In gram-negative bacteria, some multidrug efflux systems require two auxiliary constituents, which might enable drug transport to occur across both membranes of the cell envelope. These auxiliary constituents belong to the membrane fusion protein and the outer membrane factor families, respectively. This review examines in detail each of the characterized proton-linked multidrug efflux systems. The molecular basis of the broad substrate specificity of these transporters is discussed. The surprisingly wide distribution of multidrug efflux systems and their multiplicity in single organisms, with Escherichia coli, for instance, possessing at least nine proton-dependent multidrug efflux systems with overlapping specificities, is examined. We also discuss whether the normal physiological role of the multidrug efflux systems is to protect the cell from toxic compounds or whether they fulfil primary functions unrelated to drug resistance and only efflux multiple drugs fortuitously or opportunistically.
INTRODUCTION .......................................................................................................................................................233 METHODS FOR STUDYING mRNA TURNOVER IN S. CEREVISIAE ...........................................................234 Approach to Steady-State Labeling......................................................................................................................234 Inhibition of Transcription by Using Drugs .......................................................................................................234 Inhibition of Transcription by Using a Conditional Allele of RNA Polymerase II.......................................234 Inhibition of Transcription by Using Regulated Promoters.............................................................................235 Transcriptional Pulse-Chase: a Method for Examining Pathways of Decay..................................................235 Identification of Intermediates in mRNA Decay ................................................................................................235 DETERMINANTS OF mRNA STABILITY IN S. CEREVISIAE ..........................................................................236 Specific Sequences Influence mRNA Half-Lives.................................................................................................236 Nonspecific Features of mRNAs Generally Do Not Influence mRNA Half-Lives .........................................237 There is no correlation between mRNA length and stability .......................................................................237 Ribosome protection cannot account for mRNA half-lives...........................................................................237 Rare codons are not general determinants of mRNA stability ....................................................................238 A COMMON PATHWAY OF mRNA DECAY........................................................................................................238 Deadenylation Precedes the Decay of Some Yeast mRNAs ..............................................................................238 Decapping and 5*-to-3* Exonucleolytic Digestion Follow Deadenylation of Some Yeast mRNAs...............239 Deadenylation-Dependent Decapping Is a Common Pathway of mRNA Decay ............................................239 Control of mRNA Half-Lives through the Deadenylation-Dependent Decapping Pathway .........................240 Control of mRNA deadenylation ......................................................................................................................240 (i) Poly(A)-binding protein influences deadenylation................................................................................240 (ii) Poly(A)-binding protein-dependent nuclease activity from S. cerevisiae ..........................................240 (iii) Other proteins possibly involved in deadenylation............................................................................240 (iv) Models of poly(A) shortening ................................................................................................................240 (v) Terminal deadenylation is not a rate-determining step for 5*-to-3* decay ......................................241 Control of mRNA decapping .............................................................................................................................241 (i) The Pab1p-poly(A) tail complex inhibits mRNA decapping ...............................................................241 (ii) Control of decapping after deadenylation ............................................................................................242 (iii) Decapping activities from S. cerevisiae .................................................................................................242 (iv) Translation and mRNA decapping .......................................................................................................242 ADDITIONAL PATHWAYS OF mRNA DECAY IN S. CEREVISIAE .................................................................243 3*-to-5* mRNA Decay..............................................................................................................................................243 Endonucleolytic Cleavage of mRNAs ...................................................................................................................243 mRNA Surveillance: Rapid Deadenylation-Independent Decapping...............................................................243 Early nonsense codons trigger mRNA decapping ..........................................................................................243 Recognition of early nonsense codons .............................................................................................................244 (i) Specific sequences are required 3* of early nonsense codons.............................................................244 (ii) Specific upstream elements partially block nonsense codon-mediated decay .................................245 trans-Acting factors in nonsense codon-mediated mRNA decay ..................................................................245 Where in the cell does recognition of an early nonsense codon occur?......................................................246 REGULATED mRNA TURNOVER IN S. CEREVISIAE.......................................................................................246 CONCLUSIONS .........................................................................................................................................................246 REFERENCES ............................................................................................................................................................246
Over the last 25 years, a much broader range of taxonomic studies of bacteria has gradually replaced the former reliance upon morphological, physiological, and biochemical characterization. This polyphasic taxonomy takes into account all available phenotypic and genotypic data and integrates them in a consensus type of classification, framed in a general phylogeny derived from 16S rRNA sequence analysis. In some cases, the consensus classification is a compromise containing a minimum of contradictions. It is thought that the more parameters that will become available in the future, the more polyphasic classification will gain stability. In this review, the practice of polyphasic taxonomy is discussed for four groups of bacteria chosen for their relevance, complexity, or both: the genera Xanthomonas and Campylobacter, the lactic acid bacteria, and the family Comamonadaceae. An evaluation of our present insights, the conclusions derived from it, and the perspectives of polyphasic taxonomy are discussed, emphasizing the keystone role of the species. Taxonomists did not succeed in standardizing species delimitation by using percent DNA hybridization values. Together with the absence of another "gold standard" for species definition, this has an enormous repercussion on bacterial taxonomy. This problem is faced in polyphasic taxonomy, which does not depend on a theory, a hypothesis, or a set of rules, presenting a pragmatic approach to a consensus type of taxonomy, integrating all available data maximally. In the future, polyphasic taxonomy will have to cope with (i) enormous amounts of data, (ii) large numbers of strains, and (iii) data fusion (data aggregation), which will demand efficient and centralized data storage. In the future, taxonomic studies will require collaborative efforts by specialized laboratories even more than now is the case. Whether these future developments will guarantee a more stable consensus classification remains an open question.
Centro di Endocrinologia ed Oncologia Sperimentale del Consiglio Nazionale delle Ricerche, Dipartimento di Biologia e Patologia Cellulare e Molecolare ‘‘L. Califano,’’ Universita degli Studi di Napoli ‘‘Federico II,’’ I-80131 Naples, and Dipartimento di Biologia Animale e Genetica, Universita degli Studi di Firenze, I-50125 Firenze, Italy, and Departamento de Biologia, Faculdad de Ciencias, Universidad Nacional Autonoma de Mexico, Mexico 04510 D.F., Mexico
Cytokines are a diverse group of proteins and glycoproteins which have potent and wide-ranging effects on eukaryotic cell function and are now recognized as important mediators of tissue pathology in infectious diseases. It is increasingly recognized that for many bacterial species, cytokine induction is a major virulence mechanism. Until recent years, the only bacterial component known to stimulate cytokine synthesis was lipopolysaccharide (LPS). It is only within the past decade that it has been clearly shown that many components associated with the bacterial cell wall, including proteins, glycoproteins, lipoproteins, carbohydrates, and lipids, have the capacity to stimulate mammalian cells to produce a diverse array of cytokines. It has been established that many of these cytokine-inducing molecules act by mechanisms distinct from that of LPS, and thus their activities are not due to LPS contamination. Bacteria produce a wide range of virulence factors which cause host tissue pathology, and these diverse factors have been grouped into four families: adhesins, aggressins, impedins, and invasins. We suggest that the array of bacterial cytokine-inducing molecules represents a new class of bacterial virulence factor, and, by analogy with the known virulence families, we suggest the term "modulin" to describe these molecules, because the action of cytokines is to modulate eukaryotic cell behavior. This review summarizes our current understanding of cytokine biology in relation to tissue homeostasis and disease and concisely reviews the current literature on the cytokine-inducing molecules produced by gram-negative and gram-positive bacteria, with an emphasis on the cellular mechanisms responsible for cytokine induction. We propose that modulins, by controlling the host immune and inflammatory responses, maintain the large commensal flora that all multicellular organisms support.
All cells secrete a diversity of macromolecules to modify their environment or to protect themselves. Eukaryotic cells have evolved a complex secretory pathway consisting of several membrane-bound compartments which contain specific sets of proteins. Experimental work on the secretory pathway has focused mainly on mammalian cell lines or on yeasts. Now, some general principles of the secretory pathway have become clear, and most components of the secretory pathway are conserved between yeast cells and mammalian cells. However, the structure and function of the secretory system in protists have been less extensively studied. In this review, we summarize the current knowledge about the secretory pathway of five different groups of protists: Giardia lamblia, one of the earliest lines of eukaryotic evolution, kinetoplastids, the slime mold Dictyostelium discoideum, and two lineages within the "crown" of eukaryotic cell evolution, the alveolates (ciliates and Plasmodium species) and the green algae. Comparison of these systems with the mammalian and yeast system shows that most elements of the secretory pathway were presumably present in the earliest eukaryotic organisms. However, one element of the secretory pathway shows considerable variation: the presence of a Golgi stack and the number of cisternae within a stack. We suggest that the functional separation of the plasma membrane from the nucleus-endoplasmic reticulum system during evolution required a sorting compartment, which became the Golgi apparatus. Once a Golgi apparatus was established, it was adapted to the various needs of the different organisms.
T helper (Th) cells are of central importance in regulating many critical immune effector mechanisms. The profile of cytokines produced by Th cells correlates with the type of effector cells induced during the immune response to foreign antigen. Th1 cells induce the cell-mediated immune response, while Th2 cells drive antibody production. Th cells are the preferential targets of human retroviruses. Infections with human T-cell leukemia virus (HTLV) or human immunodeficiency virus (HIV) result in the expansion of Th cells by the action of HTLV (adult T-cell leukemia) or the progressive loss of T cells by the action of HIV (AIDS). Both retrovirus infections impart a high-level activation state in the host immune cells as well as systemically. However, diverging responses to this activation state have contrasting effects on the Th-cell population. In HIV infection, Th-cell loss has been attributed to several mechanisms, including a selective elimination of cells by apoptosis. The induction of apoptosis in HIV infection is complex, with many different pathways able to induce cell death. In contrast, infection of Th cells with HTLV-1 affords the cell a protective advantage against apoptosis. This advantage may allow the cell to escape immune surveillance, providing the opportunity for the development of Th-cell cancer. In this review, we will discuss the impact of Th-cell activation and general immune activation on human retrovirus expression with a focus upon Th-cell function and the progression to disease.
INTRODUCTION .......................................................................................................................................................135 AGGREGATION.........................................................................................................................................................135 Aggregation Gene Network ....................................................................................................................................137 POSTAGGREGATION...............................................................................................................................................138 Cell-Type-Specific Genes........................................................................................................................................138 Postaggregative Gene Network..............................................................................................................................139 CELL TYPE SPECIALIZATION..............................................................................................................................140 Network That Regulates Cell Type Specialization .............................................................................................141 CULMINATION..........................................................................................................................................................142 Network That Regulates Culmination .................................................................................................................145 NETWORKS OF NETWORKS.................................................................................................................................146 ACKNOWLEDGMENTS ...........................................................................................................................................147 REFERENCES ............................................................................................................................................................147
INTRODUCTION .......................................................................................................................................................216 PROBLEM POLLUTANTS AND ETHER SCISSION..........................................................................................217 Agrochemicals..........................................................................................................................................................217 Polyethers.................................................................................................................................................................218 Polyethylene glycols ............................................................................................................................................218 Polypropylene glycols and polytetramethylene glycols ..................................................................................219 Detergents ................................................................................................................................................................219 Builder compounds.............................................................................................................................................219 Alcohol ethoxylates .............................................................................................................................................219 Alkylphenol ethoxylates......................................................................................................................................220 Alkylethoxy sulfate surfactants .........................................................................................................................220 BIOCHEMICAL MECHANISMS OF ETHER CLEAVAGE................................................................................221 Oxygenation .............................................................................................................................................................221 Oxidation by Cytochromes P-450 .........................................................................................................................221 Hydroxyl Shift Mechanisms ..................................................................................................................................223 Hydrolysis ................................................................................................................................................................225 Anaerobic O Dealkylation of Alkyl-Aryl Ethers .................................................................................................225 Oxidation to Carboxylic Acids ..............................................................................................................................226 Reduction .................................................................................................................................................................227 Carbon-Oxygen Bond Cleavage by Lyases ..........................................................................................................228 CONCLUDING REMARKS......................................................................................................................................228 State of Knowledge and Prospects .......................................................................................................................228 Pathways...............................................................................................................................................................228 Enzymes................................................................................................................................................................229 Emerging Themes ...................................................................................................................................................229 Natural Substrates for Ether Cleavage Systems ................................................................................................229 ACKNOWLEDGMENT..............................................................................................................................................230 REFERENCES ............................................................................................................................................................230
INTRODUCTION AND TERMINOLOGY .............................................................................................................151 TYPES OF BACTERIAL SACs.................................................................................................................................153 SYNTHETIC SACs AND BACTERIA......................................................................................................................154 In Solution ...............................................................................................................................................................154 Sodium dodecyl sulfate ......................................................................................................................................154 Quaternary ammonium compounds.................................................................................................................154 Various surfactants.............................................................................................................................................155 Immobilized on Surfaces .......................................................................................................................................155 Insolubilized quaternary ammonium compounds ..........................................................................................155 Insolubilized block copolymer surfactants ......................................................................................................155 Miscellaneous Effects .............................................................................................................................................156 BACTERIAL SACs AND BACTERIA ......................................................................................................................156 Physiological Roles .................................................................................................................................................156 Other Observations ................................................................................................................................................157 Applied Aspects of Bacterial SACs.......................................................................................................................157 SURFACE-ACTIVE APPROACH TO BACTERIAL ADHESION/DEADHESION............................................157 SIGNIFICANCE OF BACTERIAL SACs IN ADHESION TO INTERFACES ..................................................158 SACs Bound at the Bacterial Cell Surface .........................................................................................................158 Cell-bound biosurfactants..................................................................................................................................158 Cell-bound polymeric SACs...............................................................................................................................159 SACs Bound at the Substratum ...........................................................................................................................159 Excreted biosurfactants......................................................................................................................................159 Excreted polymeric SACs...................................................................................................................................160 SIGNIFICANCE OF BACTERIAL SACs IN DEADHESION FROM INTERFACES ......................................160 Biosurfactants..........................................................................................................................................................160 Polymeric SACs.......................................................................................................................................................161 GLIDING—A CONTINUOUS DEADHESION WITHIN TWO DIMENSIONS ...............................................161 BACTERIAL CELL SURFACE HYDROPHOBICITY—REGULATION VIA BACTERIAL SACs?...............161 CONCLUSIONS .........................................................................................................................................................162 ACKNOWLEDGMENTS ...........................................................................................................................................162 REFERENCES ............................................................................................................................................................162
