Analysis of the polar lipids of many pathogenic and non-pathogenic clostridia has revealed the presence of plasmalogens, alk-1′-enyl ether-containing phospholipids and glycolipids. An exception to this finding so far has been Clostridium difficile, an important human pathogen which is the cause of antibiotic-associated diarrhea and other more serious complications. We have examined the polar lipids of three strains of C. difficile by thin-layer chromatography and have found acid-labile polar lipids indicative of the presence of plasmalogens. The lipids from one of these strains were subjected to further analysis by liquid chromatography coupled to electrospray ionization-mass spectrometry (LC/ESI-MS), which revealed the presence of phosphatidylglycerol, cardiolipin, monohexosyldiradylglycerol, dihexosyldiradylglycerol, and two unusual glycolipids identified as an aminohexosyl-hexosyldiradylglycerol, and a trihexosyldiradylglycerol. High resolution tandem mass spectrometry determined that monohexosyldiradylglycerol, cardiolipin and phosphatidylglycerol contained significant amounts of plasmalogens. C. difficile thus joins the growing list of clostridia that have plasmalogens. Since plasmalogens in clostridia are formed by an anaerobic pathway distinct from that in animal cells, their formation represents a potential novel target for antibiotic action.
bQuorum sensing (QS) is widely used by bacteria to coordinate behavior in response to external stimuli. In Vibrio cholerae, this process is important for environmental survival and pathogenesis, though, intriguingly, a large percentage of natural isolates are QS deficient. Here, we show that QS-deficient mutants can spread as social cheaters by ceasing production of extracellular proteases under conditions requiring their growth. We further show that mutants stimulate biofilm formation and are over-represented in biofilms compared to planktonic communities; on this basis, we suggest that QS-deficient mutants may have the side effect of enhancing environmental tolerance of natural populations due to the inherent resistance properties of biofilms. Interestingly, high frequencies of QS-deficient individuals did not impact production of QS signaling molecules despite mutants being unable to respond to these inducers, indicating that these variants actively cheat by false signaling under conditions requiring QS. Taken together, our results suggest that social cheating may drive QS deficiency emergence within V. cholerae natural populations.
Mutualisms are common in nature, though these symbioses can be quite permeable to cheaters in situations where one individual parasitizes the other by discontinuing cooperation yet still exploits the benefits of the partnership. In the Rhizobium-legume system, there are two separate contexts, namely nodulation and nitrogen fixation processes, by which resident Rhizobium individuals can benefit by cheating. Here, we constructed reversible and irreversible mutations in key nodulation and nitrogen-fixation pathways of Rhizobium etli and compared their interaction with plant hosts Phaseolus vulgaris to that of wild type. We show that R. etli reversible mutants deficient in nodulation factor production are capable of intra-specific cheating, wherein mutants exploit other Rhizobium individuals capable of producing these factors. Similarly, we show that R. etli mutants are also capable of cheating inter-specifically, colonizing the host legume yet contributing nothing to the partnership in terms of nitrogen fixation. Our findings indicate that cheating is possible in both of these frameworks, seemingly without damaging the stability of the mutualism itself. These results may potentially help explain observations suggesting that legume plants are commonly infected by multiple bacterial lineages during the nodulation process.
Vibrio cholerae is the causative agent of the devastating diarrheal disease cholera. A number of regulatory pathways are involved in V. cholerae pathogenesis and antibiotic resistance. For example, there are over 40 LysR-family proteins in the V. cholerae genome, but most of their functions are unknown. In this study, we examine the role of VC2323 (TehAVc) and its divergently transcribed LysR-family regulator VC2324 (TehRVc) in V. cholerae pathogenesis. We found that in V. cholerae C6706, the expression of tehAVc is dependent on TehRVc. VC2323 (TehAVc), homologous to the Escherichia coli tellurite resistance protein (TehAEc), differs from TehAEc in that TehAVc has no noticeable role in tellurite resistance but instead contributes to chloramphenicol resistance. Interestingly, both tehAVc and tehRVc mutants were defective in colonization of infant mice. Though the expression of a key virulence gene tcpA was not affected in either of these mutants, tehAVc mutants failed to attach to mouse intestinal surfaces in the presence of crude bile, suggesting a new role of the TehAVc-TehRVc pair in V. cholerae pathogenesis.
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