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• W4246645615 abstract "Bacteria use a variety of means to communicate with one another and with their eukaryotic hosts. In some cases, social interactions allow bacteria to synchronize the behavior of all of the members of the group and thereby act like multicellular organisms. By contrast, some bacterial social engagements promote individuality among members within the group and thereby foster diversity. Here we explore the molecular mechanisms underpinning some recently discovered bacterial communication systems. These include long- and short-range chemical signaling channels; one-way, two-way, and multi-way communication; contact-mediated and contact-inhibited signaling; and the use and spread of misinformation or, more dramatically, even deadly information. Bacteria use a variety of means to communicate with one another and with their eukaryotic hosts. In some cases, social interactions allow bacteria to synchronize the behavior of all of the members of the group and thereby act like multicellular organisms. By contrast, some bacterial social engagements promote individuality among members within the group and thereby foster diversity. Here we explore the molecular mechanisms underpinning some recently discovered bacterial communication systems. These include long- and short-range chemical signaling channels; one-way, two-way, and multi-way communication; contact-mediated and contact-inhibited signaling; and the use and spread of misinformation or, more dramatically, even deadly information. In the 300 years since van Leeuwenhoek's remarkable descriptions of the teeming world of microorganisms, bacteria have been regarded as deaf mutes going about their business without communicating with their neighbors. It was not until the 1960s and 1970s, with the discovery of what is now called quorum sensing, that it became evident that bacteria possess sophisticated systems of communication that enable them to send and receive chemical messages to and from other bacteria. In its simplest form, quorum sensing is a cell-cell communication mechanism by which bacteria count their own numbers by producing and detecting the accumulation of a signaling molecule that they export into their environment. We now know that quorum-sensing-mediated communication is more complicated than originally assumed and, furthermore, is but one of several mechanisms bacteria use to interact with other cells. Here, following a brief review of quorum sensing, we summarize recent developments in the field of cell-cell communication and interaction among bacteria and between bacteria and eukaryotes.The number of these Animals [bacteria] in the scurf of a man's Teeth are so many that I believe they exceed the number of Men in a kingdom. For upon the examination of a small parcel of it, no thicker than a Horse-hair, I found too many living Animals therein, that I guess there might have been 1000 in a quantity of matter no bigger than the 1/100 part of a sand.—Antony van Leeuwenhoek, 1684 The concept of intercellular communication within a bacterial population originates with the discoveries of Tomasz (Tomasz, 1965Tomasz A. Control of the competent state in Pneumococcus by a hormone-like cell product: an example for a new type of regulatory mechanism in bacteria.Nature. 1965; 208: 155-159Crossref PubMed Scopus (141) Google Scholar) on genetic competence in Streptococcus pneumoniae (then known as Pneumococcus) and Hastings (Nealson et al., 1970Nealson K.H. Platt T. Hastings J.W. Cellular control of the synthesis and activity of the bacterial luminescent system.J. Bacteriol. 1970; 104: 313-322Crossref PubMed Google Scholar) on bioluminescence in Vibrio. Competence is a physiological state in which bacteria are capable of taking up and undergoing genetic transformation by DNA molecules. In 1965, Tomasz reported that entry into the competent state is governed by an extracellular factor that is manufactured by Streptococcus itself (Tomasz, 1965Tomasz A. Control of the competent state in Pneumococcus by a hormone-like cell product: an example for a new type of regulatory mechanism in bacteria.Nature. 1965; 208: 155-159Crossref PubMed Scopus (141) Google Scholar). Thus, the competence factor, which was later shown to be a modified peptide (below), was described as a “hormone-like activator” that synchronizes the behavior of the bacterial population. In 1970, Hastings showed that two obscure species of bioluminescent marine bacteria, Vibrio fischeri and Vibrio harveyi, produced light at high cell density but not in dilute suspensions (Nealson et al., 1970Nealson K.H. Platt T. Hastings J.W. Cellular control of the synthesis and activity of the bacterial luminescent system.J. Bacteriol. 1970; 104: 313-322Crossref PubMed Google Scholar). Light production could be stimulated by the exogenous addition of cell-free culture fluids, and the component responsible, called the autoinducer, was later identified as an acyl-homoserine lactone (AHL; Eberhard et al., 1981Eberhard A. Burlingame A.L. Eberhard C. Kenyon G.L. Nealson K.H. Oppenheimer N.J. Structural identification of autoinducer of Photobacterium fischeri luciferase.Biochemistry. 1981; 20: 2444-2449Crossref PubMed Scopus (640) Google Scholar) (Figure 1). The combined findings of Tomasz and Hastings suggested that certain bacteria use the production, release, exchange, and detection of signaling molecules to measure their population density and to control their behavior in response to variations in cell numbers. For nearly 20 years, these cell-cell signaling phenomena were considered anomalous occurrences restricted to a few specialized bacteria. It is now clear that intercellular communication is not the exception but, rather, is the norm in the bacterial world and that this process, called quorum sensing, is fundamental to all of microbiology. How does quorum sensing work? As a population of quorum-sensing bacteria grows, a proportional increase in the extracellular concentration of the signaling molecule occurs. When a threshold concentration is reached, the group detects the signaling molecule and responds to it with a population-wide alteration in gene expression (Figure 2A). Processes controlled by quorum sensing are usually ones that are unproductive when undertaken by an individual bacterium but become effective when undertaken by the group. For example, in addition to competence and bioluminescence, quorum sensing controls virulence factor secretion, biofilm formation, and sporulation. Thus, quorum sensing is a mechanism that allows bacteria to function as multicellular organisms and to reap benefits that they could never obtain if they always acted as loners. A chemical vocabulary has been established in which Gram-negative quorum-sensing bacteria such as Vibrio communicate with AHLs, which are the products of LuxI-type autoinducer synthases. These small molecules are detected by cognate cytoplasmic LuxR proteins that, upon binding their partner autoinducer, bind DNA and activate transcription of target quorum-sensing genes. By contrast, Gram-positive quorum-sensing bacteria, such as Streptococcus and Bacillus, predominantly communicate with short peptides that often contain chemical modifications. For example, the signaling molecule for genetic competence in B. subtilis ComX is a 6 amino acid peptide whose tryptophan residue has been modified by the attachment of a geranyl group (Figure 1; Okada et al., 2005Okada M. Sato I. Cho S.J. Iwata H. Nishio T. Dubnau D. Sakagami Y. Structure of the Bacillus subtilis quorum-sensing peptide phereomone ComX.Nat. Chem. Biol. 2005; 1: 23-24Crossref PubMed Scopus (98) Google Scholar). Signaling peptides such as ComX are recognized by membrane bound two-component sensor histidine kinases. Signal transduction occurs by phosphorylation cascades that ultimately impinge on DNA binding transcription factors responsible for regulation of target genes. In general, bacteria keep their AHL and peptide quorum-sensing conversations private by each speacies of bacteria producing and detecting a unique AHL (AHLs differ in their acyl side-chain moieties), peptide, or combination thereof. AHLs and peptides represent the two major classes of known bacterial cell-cell signaling molecules. However, our appreciation of the complexity of the chemical lexicon is increasing as new molecules are discovered that convey information between cells. For example, a family of molecules generically termed autoinducer-2 (AI-2) has been found to be widespread in the bacterial world and to facilitate interspecies communication. AI-2s are all derived from a common precursor, 4,5-dihydroxy-2,3 pentanedione (DPD), the product of the LuxS enzyme (Figure 1). DPD undergoes spontaneous rearrangements to produce a collection of interconverting molecules, some (and perhaps all) of which encode information (Xavier and Bassler, 2005Xavier K.B. Bassler B.L. Interference with AI-2-mediated bacterial cell-cell communication.Nature. 2005; 437: 750-753Crossref PubMed Scopus (218) Google Scholar). Presumably, AI-2 interconversions allow bacteria to respond to endogenously produced AI-2 and also to AI-2 produced by other bacterial species in the vicinity, giving rise to the idea that AI-2 represents a universal language: a “Bacterial Esperanto.” AI-2, often in conjunction with an AHL or oligopeptide autoinducer, controls a variety of traits in different bacteria ranging from bioluminescence in V. harveyi to growth in Bacillus anthracis to virulence in Vibrio cholerae and many other clinically relevant pathogens. The streptomycetes, common soil-dwelling Gram-positive bacteria, use γ-butyrolactones (Figure 1) to control morphological differentiation and secondary metabolite production. The best studied of these signals, A-factor of Streptomyces griseus (one of the earliest recognized signaling molecules in bacteria), antagonizes a DNA binding repressor protein, ArpA, thereby promoting the formation of hair-like projections known as aerial hyphae and the production of the antibiotic streptomycin (Khokhlov et al., 1967Khokhlov A.S. Tovarova I.I. Borisova L.N. Pliner S.A. Schevchenko L.A. Kornitskaya E.Y. Ivkina N.S. Rappoport I.A. A-factor responsible for the biosynthesis of streptomycin by a mutant strain of Actinomyces streptomycini.Dokl. Akad. Nauk SSSR. 1967; 177: 232-235PubMed Google Scholar, Onaka et al., 1995Onaka H. Ando N. Nihira T. Yamada Y. Beppu T. Horinouchi S. Cloning and characterization of the A-factor receptor gene from Streptomyces griseus.J. Bacteriol. 1995; 177: 6083-6092Crossref PubMed Google Scholar). Interestingly, γ-butyrolactones are structural analogs of AHLs; however, no crossrecognition of signals has been cited to date. Myxococcus xanthus, another soil bacterium, employs a mixture of amino acids derived from extracellular proteolysis as signaling molecules (Kuspa et al., 1992Kuspa A. Plamann L. Kaiser D. Identification of heat-stable A-factor from Myxococcus xanthus.J. Bacteriol. 1992; 174: 3319-3326PubMed Google Scholar). M. xanthus monitors the environment for the simultaneous presence of starvation conditions and trace amounts of certain amino acids (a mixture of tryptophan, proline, tyrosine, phenylalanine, leucine, and isoleucine is especially potent) prior to initiating the quorum-sensing cascade that culminates in a spore-filled fruiting body (discussed further below). Other molecules, including 3-OH palmitic acid methyl ester, cyclic dipeptides, and quinolones (see below), also have roles in bacterial cell-cell signaling (for review, see Waters and Bassler, 2005Waters C.M. Bassler B.L. Quorum sensing: cell-to-cell communication in bacteria.Annu. Rev. Cell Dev. Biol. 2005; 21: 319-346Crossref PubMed Scopus (2476) Google Scholar). Some quorum-sensing molecules, such as the quinolone signal (2-heptyl-3-hydroxy-4-quinolone) of Pseudomonas aeruginosa (PQS for Pseudomonas quinolone signal, Figure 1), are extremely hydrophobic (Pesci et al., 1999Pesci E.C. Milbank J.B. Pearson J.P. McKnight S. Kende A.S. Greenberg E.P. Iglewski B.H. Quinolone signaling in the cell-to-cell communication system of Pseudomonas aeruginosa.Proc. Natl. Acad. Sci. USA. 1999; 96: 11229-11234Crossref PubMed Scopus (785) Google Scholar). This is problematic because PQS must travel from cell to cell in an aqueous environment. How does P. aeruginosa manage to disperse a water-insoluble signaling molecule in water? A solution to this mystery was recently reported (Mashburn and Whiteley, 2005Mashburn L.M. Whiteley M. Membrane vesicles traffic signals and facilitate group activities in a prokaryote.Nature. 2005; 437: 422-425Crossref PubMed Scopus (496) Google Scholar). In a process reminiscent of eukaryotic packaging of cargo into vesicles that are trafficked between organelles, Gram-negative bacteria, such as Pseudomonas, pinch off 0.5 μm-sized vesicles from their outer membranes, and often these vesicles transport various kinds of macromolecules. Mashburn and Whiteley find that Pseudomonas packages PQS into vesicles derived from the bacterial membrane and the vesicles deliver the quinolones to neighboring cells (Figure 2B). Remarkably, PQS mediates its own packaging; mutants blocked in quinolone production fail to produce membrane vesicles but regain the capacity to do so when chemically synthesized PQS is supplied exogenously (Mashburn and Whiteley, 2005Mashburn L.M. Whiteley M. Membrane vesicles traffic signals and facilitate group activities in a prokaryote.Nature. 2005; 437: 422-425Crossref PubMed Scopus (496) Google Scholar). In addition to PQS, the Pseudomonas vesicles contain other quinolones that function as antibiotics to kill other species of bacteria, such as Staphylococcus epidermidis. Thus, P. aeruginosa sends mixed messages: To its own kind, it emits signals that foster group behavior, but to other kinds of bacteria, the message delivered is fatal (Figure 2B). Recent discoveries of quorum-quenching mechanisms suggest that biological tit-for-tat matches have evolved for counteracting quorum-sensing bacteria. Presumably, anti-quorum-sensing strategies are deployed so that one species of bacteria can outcompete another quorum-sensing species or so that a eukaryote can fend off a quorum-sensing bacterial invader (Figure 2C). One such activity was discovered in soil samples assayed for interference with AHL detection and response in a promiscuous AHL quorum-sensing-responsive reporter strain. The inhibitory activity was defined as a lactonase enzyme, AiiA, which cleaves the acyl moiety from the lactone rings of AHLs (Dong et al., 2000Dong Y.H. Xu J.L. Li X.Z. Zhang L.H. AiiA, an enzyme that inactivates the acylhomoserine lactone quorum-sensing signal and attenuates the virulence of Erwinia carotovora.Proc. Natl. Acad. Sci. USA. 2000; 97: 3526-3531Crossref PubMed Scopus (682) Google Scholar). AiiA is especially nonspecific with regard to acyl side chains, so it is believed to inactivate many AHL autoinducers. AiiA production is attributed to a variety of Bacillus species, which is noteworthy because Bacillus spp. are Gram-positive bacteria and use peptide autoinducers to communicate. Thus, Bacillus renders the Gram-negative bacterial community mute while managing to continue its own conversations uninterrupted. Analogous strategies have since been discovered. In a particularly insidious scheme, Variovorax paradoxus destroys AHLs with an AHL-degrading enzyme that functions by ring opening; after disabling quorum sensing in its foes, V. paradoxus consumes the linearized product and uses it to acquire carbon and nitrogen (Leadbetter and Greenberg, 2000Leadbetter J.R. Greenberg E.P. Metabolism of acyl-homoserine lactone quorum-sensing signals by Variovorax paradoxus.J. Bacteriol. 2000; 182: 6921-6926Crossref PubMed Scopus (371) Google Scholar). It remains to be established whether AHL degradation has significant consequences for bacterial signaling in the natural environment. Interference with peptide signaling is also well known. Staphylococcus aureus relies on peptide quorum sensing for virulence, and strains of this pathogen are grouped according to the autoinducing peptide that they produce. Each autoinducing peptide, while activating the quorum-sensing cascade of the group that produces it, crossinhibits quorum sensing in the other groups (Figure 2C). The autoinducing peptides are extremely similar in structure, and crossinhibition occurs because the different peptides compete for binding to the autoinducer receptors (Lyon et al., 2002Lyon G.J. Wright J.S. Christopoulos A. Novick R.P. Muir T.W. Reversible and specific extracellular antagonism of receptor-histidine kinase signaling.J. Biol. Chem. 2002; 277: 6247-6253Crossref PubMed Scopus (74) Google Scholar). Presumably, in mixed infections, the S. aureus group that is first to successfully establish its quorum-sensing cascade shuts down quorum sensing in the other groups and becomes the predominant group to colonize the host. This has been borne out in in vivo mouse abscess models in which mice injected with a particular S. aureus group are susceptible to infection, but not if the S. aureus group is coinjected with the autoinducing peptide from another S. aureus group (Wright et al., 2005Wright 3rd, J.S. Jin R. Novick R.P. Transient interference with staphylococcal quorum sensing blocks abscess formation.Proc. Natl. Acad. Sci. USA. 2005; 102: 1691-1696Crossref PubMed Scopus (197) Google Scholar). Quorum-sensing interference has been reported for AI-2-mediated communication. Some bacteria, such as Escherichia coli and Salmonella typhimurium, possess AI-2-specific importers that are induced in response to high levels of AI-2 in the environment. AI-2 import eliminates the signal from the extracellular environment. In mixed-species consortia, because AI-2 molecules spontaneously interconvert, bacteria with AI-2 importers can consume both their own AI-2 and that produced by other species in the vicinity. This capability enables AI-2-consuming bacteria to interfere with other species' ability to accurately count the cell density of the population and to appropriately respond to changes in it (Xavier and Bassler, 2005Xavier K.B. Bassler B.L. Interference with AI-2-mediated bacterial cell-cell communication.Nature. 2005; 437: 750-753Crossref PubMed Scopus (218) Google Scholar). Eukaryotes too appear to possess armaments that are specifically aimed at quorum-sensing bacteria. The seaweed Delisea pulchra produces halogenated furanones that are structural analogs of AHLs. These molecules bind to LuxR-type transcription factors and cause their proteolysis (Manefield et al., 2002Manefield M. Rasmussen T.B. Henzter M. Andersen J.B. Steinberg P. Kjelleberg S. Givskov M. Halogenated furanones inhibit quorum sensing through accelerated LuxR turnover.Microbiol. 2002; 148: 1119-1127PubMed Google Scholar). Reactive oxygen and nitrogen intermediates produced by NADPH oxidase, an important constituent of the mammalian immune system, inactivate S. aureus autoinducing peptides in a mouse virulence model system (Rothfork et al., 2004Rothfork J.M. Timmins G.S. Harris M.N. Chen X. Lusis A.J. Otto M. Cheung A.L. Gresham H.D. Inactivation of a bacterial virulence pheromone by phagocyte-derived oxidants: new role for the NADPH oxidase in host defense.Proc. Natl. Acad. Sci. USA. 2004; 101: 13867-13872Crossref PubMed Scopus (84) Google Scholar). Paraoxonase enzymes hydrolyze esters and, in humans, are considered to have important antiatherogenic functions. The human paraoxonase (PON) family has three members: PON1, PON2, and PON3. Although their endogenous substrates have not been defined, it is clear that they are lactonases. At least PON2 is capable of inactivating a variety of bacterial AHL autoinducers, suggesting that humans possess anti-quorum-sensing capabilities (Draganov et al., 2005Draganov D.I. Teiber J.F. Speelman A. Osawa Y. Sunahara R. La Du B.N. Human paraoxonases (PON1, PON2, and PON3) are lactonases with overlapping and distinct substrate specificities.J. Lipid Res. 2005; 46: 1239-1247Crossref PubMed Scopus (510) Google Scholar). However, a direct in vivo link between PON2 and AHL inactivation awaits experimental verification. Some bacteria, as we have discussed, converse over a distance by exchanging diffusible signals that allow members of a community of cells to communicate (quorum sensing). At the opposite extreme are short-range signals that require direct contact between individual cells for information exchange. One classic example of this is C signaling, which is critical for multicellular fruiting-body formation by M. xanthus (Figure 3A). Cells of this social bacterium move on surfaces by gliding motility in a manner in which individual cells often reverse direction. C signaling promotes a coordinated gliding behavior known as streaming, in which reversals are suppressed. Streaming culminates in the formation of a mound of cells within which spore formation takes place. The C signal is a 17 kDa protein that is derived by proteolysis from a larger precursor (Kim and Kaiser, 1990aKim S.K. Kaiser D. C-factor: a cell-cell signaling protein required for fruiting body morphogenesis of M. xanthus.Cell. 1990; 61: 19-26Abstract Full Text PDF PubMed Scopus (149) Google Scholar, Kim and Kaiser, 1990cKim S.K. Kaiser D. Purification and properties of Myxococcus xanthus C-factor, an intercellular signaling protein.Proc. Natl. Acad. Sci. USA. 1990; 87: 3635-3639Crossref PubMed Scopus (63) Google Scholar, Lobedanz and Sogaard-Andersen, 2003Lobedanz S. Sogaard-Andersen L. Identification of the C-signal, a contact-dependent morphogen coordinating multiple developmental responses in Myxococcus xanthus.Genes Dev. 2003; 17: 2151-2161Crossref PubMed Scopus (96) Google Scholar). Elegant experiments in which cells were artificially forced into alignment in tiny grooves on an agar plate showed that C signaling requires contact between cells. It has been hypothesized that the function of C signaling is to report on cell alignment, which takes place during the aggregation phase of fruiting-body formation (Julien et al., 2000Julien B. Kaiser A.D. Garza A. Spatial control of cell differentiation in Myxococcus xanthus.Proc. Natl. Acad. Sci. USA. 2000; 97: 9098-9103Crossref PubMed Scopus (177) Google Scholar, Kim and Kaiser, 1990bKim S.K. Kaiser D. Cell alignment required in differentiation of Myxococcus xanthus.Science. 1990; 249: 926-928Crossref PubMed Scopus (121) Google Scholar). C signaling also governs the expression of numerous genes required for spore formation. A cell-surface receptor (perhaps located at the cell poles) is presumed to be required for C signaling, but the putative receptor and the downstream signal-transduction system remain unknown. The concept that M. xanthus cells are capable of intimate interaction is reinforced by the recent dramatic demonstration that particular motility-associated, GFP-tagged outer-membrane lipoproteins readily exchange between M. xanthus cells (Nudleman et al., 2005Nudleman E. Wall D. Kaiser D. Cell-to-cell transfer of bacterial outer membrane lipoproteins.Science. 2005; 309: 125-127Crossref PubMed Scopus (110) Google Scholar). This finding suggests that M. xanthus cells are, at a minimum, capable of at least briefly fusing their outer membranes and sharing outer-membrane proteins. Exactly how C signaling suppresses gliding reversals remains largely unknown, but an important insight comes from recent cytological studies on the protein FrzS, which is required for directed movement (Mignot et al., 2005Mignot T. Merlie Jr., J.P. Zusman D.R. Regulated pole-to-pole oscillations of a bacterial gliding motility protein.Science. 2005; 310: 855-857Crossref PubMed Scopus (96) Google Scholar). Gliding is mediated by fiber-like pili that extend from one end of the cell and use their tips like a harpoon to latch on to the substratum or another cell. Movement is subsequently achieved by retraction of the pili. The bacteria reverse direction by disassembling pili at one cell pole and reassembling pili at the other pole. FrzS oscillates from pole to pole, evidently traveling along an undefined, cytoskeletal track. Conceivably, FrzS is part of a pilus-assembly complex that alternately governs pilus construction at one pole and then the other. If so, a downstream consequence of C signaling might be suppression of this pole-to-pole oscillation. An extreme example of intimate cell-to-cell signaling occurs during the process of spore formation in Bacillus subtilis. Spores are formed in a two-chamber sporangium that consists of a forespore that ultimately becomes the spore and a mother cell that nurtures the developing spore. Early in sporulation, the forespore and mother cell lie side by side, but later in development, the mother cell wholly engulfs the forespore to create a cell within a cell. Thus, during sporulation, the forespore and the mother cell are in intimate contact across the membranes where the cells abut each other. Each of these cells follows its own distinctive program of gene expression, but the two lines of gene expression are not independent of one another. Rather, they are linked in crisscross fashion by three intercellular signaling pathways (Figure 3B and Figure 4A; for reviews, see Losick and Stragier, 1992Losick R. Stragier P. Crisscross regulation of cell-type-specific gene expression during development in B. subtilis.Nature. 1992; 355: 601-604Crossref PubMed Scopus (279) Google Scholar, Rudner and Losick, 2001Rudner D.Z. Losick R. Morphological coupling in development: lessons from prokaryotes.Dev. Cell. 2001; 1: 733-742Abstract Full Text Full Text PDF PubMed Scopus (73) Google Scholar). A secreted signaling protein (SpoIIR) produced in the forespore under the control of the forespore transcription factor σF triggers the appearance of σE in the mother cell. Next, σE sets in motion a poorly understood chain of events that activates σG in the forespore. Finally, σG directs the synthesis of SpoIVB, a secreted signaling protein that triggers the appearance of σK in the mother cell. A case of an “in your face” conversation is contact-mediated growth inhibition in E. coli (Aoki et al., 2005Aoki S.K. Pamma R. Hernday A.D. Bickham J.E. Braaten B.A. Low D.A. Contact-dependent inhibition of growth in Escherichia coli.Science. 2005; 309: 1245-1248Crossref PubMed Scopus (272) Google Scholar). Certain wild strains of E. coli inhibit the growth of standard laboratory strains (E. coli K12) by a mechanism known as contact-dependent inhibition. Inhibition is mediated by a pair of proteins called CdiA and CdiB (for contact-dependent inhibitors A and B) that resemble two-partner secretion proteins that are exported to the cell surface by a pathway involving proteolytic processing. When the genes for CdiA and CdiB are introduced into E. coli K12, the laboratory strain acquires the capacity to cause growth inhibition in a manner that requires cell-to-cell contact (Figure 3C and Figure 4B). Contact dependence was demonstrated in an elegant experiment in which the inhibitory cells were separated from the sensitive cells by a porous membrane. Pores of 0.4 μm prevented growth inhibition, whereas pores of 0.8 μm (large enough to allow cells to slip through) did not. Furthermore, inhibitory cells were shown to form aggregates with sensitive cells in a manner that depended on the Cdi proteins. Importantly, sensitive cells displaying surface pili are resistant to growth inhibition, presumably because the pili keep the inhibitory cells at a safe distance. The physiological significance of contact-dependent inhibition is unclear, but an attractive possibility is that it functions in the regulation of growth of specific cells in complex communities of bacteria. Most of the examples we have considered so far involve interactions among large numbers of bacteria in populations existing in liquid environments. Many bacteria are also capable of coordinating their behavior to form sessile communities consisting of large numbers of densely packed cells. These architecturally complex communities, called biofilms, form on surfaces or at air-liquid interfaces. Cells in biofilms are typically held together by an extracellular matrix composed of polysaccharides, protein, and often DNA. As in communes, all of the members of these bacterial communities cooperate in the construction of the biofilm by contributing matrix components. An interesting twist on communal living has recently been reported in Vibrio cholerae, the causative agent of cholera (Meibom et al., 2005Meibom K.L. Blokesch M. Dolganov N.A. Wu C.Y. Schoolnik G.K. Chitin induces natural competence in Vibrio cholerae.Science. 2005; 310: 1824-1827Crossref PubMed Scopus (417) Google Scholar). V. cholerae exists both free swimming in the ocean and also as a constituent of biofilms, frequently on chitin-containing exoskeletons. V. cholerae feeds on this solid polymer of N-acetylglucosamine, during which time it acquires DNA by natural transformation (DNA is known to be present in biofilms at concentrations above 100 μg/ml). DNA uptake from the environment is postulated to allow V. cholerae to obtain new genes, thereby diversifying its genome. Genes encoding type IV pili and homologs of genes required for genetic competence in Gram-positive bacteria are induced in the presence of chitin and are necessary for V. cholerae transformation. An intact quorum-sensing cascade is also a prerequisite for transformation on chitin. These studies demonstrate for the first time that V. cholerae has natural competence, that bacterial evolution could be occurring on interfaces in which bacteria are in direct contact with surfaces, and finally that this process is driven by cell-cell signaling. Another fascinating example of communal living is involved in aerial mycelium formation in streptomycetes, fungus-like bacteria that undergo a complex process of morphological" @default.
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• W4246645615 title "Bacterially Speaking" @default.
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