A number of bacteria, including some significant pathogens, utilize N-acylhomoserine lactones (AHLs) as quorum sensing signals. There is considerable interest in the therapeutic potential of disrupting quorum sensing. Recently, a number of bacteria have been identified which are capable of enzymic inactivation of AHLs. These enzymes show considerable promise as 'quenchers' of quorum sensing. However, the assumption that the natural function of these enzymes is to disrupt or modulate quorum sensing has yet to be established. This review surveys the progress made to date in this field and examines what implications these findings have for our understanding of the role played by these enzymes in vivo.
The nematode-bacterium complex of Heterorhabditis-Photorhabdus is pathogenic to insect larvae. The bacteria undergo a form of phenotypic switching whereby the primary form, at the stationary phase of the growth cycle, makes a range of products and has the capacity to support nematode growth, whereas the secondary form does not express these phenotypes. The work described here investigated the mechanism regulating phenotypic variation by transforming the primary cells with secondary-form DNA on a low-copy-number vector and screening for colonies which did not produce the yellow pigment characteristic of primaries. Four transformants all carrying the same gene were found to loose primary-form-specific characteristics, and the gene was sequenced and identified as ner, a regulatory gene in gram-negative bacteria and their phages. Unexpectedly, inactivation of the endogenous gene in the secondaries did not cause them to revert to the primary phenotype, and the gene was expressed in the primary form as well as the secondary form during exponential but not stationary phase and deregulated in the plasmid-bearing primary form. These and other pieces of evidence indicate that the endogenous ner gene is not responsible for the secondary phenotype, but that ner, when overexpressed, can repress expression of primary phenotypes at stationary phase. Inactivation of the endogenous ner gene in the primary form affected the outer membrane protein profile. A number of outer membrane proteins displayed differential accumulation in the primary and secondary forms at stationary phase, and two of the primary-form-specific proteins were absent from the ner primary strain.Photorhabdus and Xenorhabdus spp. are bacteria (family Enterobacteriaceae) carried symbiotically in the gut of nematodes of the genera Heterorhabditis and Steinernema, respectively. The nematode and bacteria act together to kill a range of insect prey (pathogenicity mechanisms reviewed in reference 10) and are used in biological pest control. In addition to producing an insecticidal toxin, the bacteria are needed for growth and reproduction of the nematodes (27). The strain used in this work fell originally into the species Xenorhabdus luminescens, which was then reclassified as a new genus with a single species, Photorhabdus luminescens. Recent taxonomic work (13) has divided Photorhabdus into three species, and the K122 strain used in this work probably falls into the P. temperata species (36
Aims: A search was conducted for a difference in genome composition between phenotypic variants of the insect pathogenic bacteria, Photorhabdus temperata.
Methods: An unstable 300 bp fragment of DNA was identified by amplified fragment length polymorphism (AFLP) analysis, which was not, however, associated with phenotypic variation.
Results: During prolonged culturing of the bacteria, one copy of the repeated fragment was deleted and a restriction site linked to one of the copies was lost or gained. The sequence did not show substantial identity to any in the database, but a 16‐bp region was identical to part of the marR gene of Escherichia coli.
Significance and Impact of the Study: The work has implications for the understanding of genetic instability in this and other pathogenic species of bacteria. In addition, the complete unstable element may be useful as a genetic tool in Photorhabdus spp.
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