resulted in the identification of another biofilm inhibitor, ursolic acid that is not toxic to E. coli and other bacteria as well as to hepatocytes. Whole transcriptome analysis showed ursolic acid ATPase pathway induced genes related to chemotaxis and motility, heat shock response, and unknown functions and that ursolic acid repressed genes related to cysteine synthesis and sulfur metabolism, however, the anti biofilm effect of ursolic acid was not related to AI 2. This manuscript and one by Rather and co workers showed sulfur metabolism is related to biofilm formation as mutations in both cysB and cysE increase biofilm formation. A related compound, asiatic acid, was found to be even more effective than ursolic acid and whole transcriptome studies showed it also involves sulfur metabolism.
Furthermore, aqueous fish muscle extract, composed primarily of fish muscle tropomyosin, was shown recently to significantly decrease attachment Droxinostat of a range of E. coli that cause urinary tract infections. Toxin/anti toxin pairs Toxin antitoxin pairs consist of a stable toxin and a labile antitoxin. T AT pairs appear to be involved in anti phage defense and other possible functions include genomic junk, growth rate control, programmed cell death, and persister formation. The value of T AT pairs to the cell has been questioned since after deleting five TAT pairs, it was shown the five best studied E. coli T AT pairs do not influence bacterial fitness of planktonic cells. However, MqsR is highly toxic since a deletion of the anti toxin B3021 is lethal, and it appears MqsR is part of a T AT pair that consists of MqsR and B3021.
Since MqsR has been linked to biofilm formation via AI 2 and via McbR, T AT pairs are clearly important for biofilm formation. In addition, deletion of the five best studied E. coli T AT pairs also alters biofilm formation, this illustrates importance of studying biofilm cells along with planktonic cells. Further evidence of this link between T AT pairs and biofilm formation is provided by Hha and YbaJ . Both Hha and TomB are highly induced in biofilms as found by whole transcriptome profiling, and Hha expression is toxic and TomB diminishes its toxicity. Hha decreases biofilm formation by repressing type I fimbriae via fimA and ihfA and by inhibiting their translation via rare tRNAs. Hha expression also induces ClpP and ClpX proteases that degrade many antitoxins, allowing free toxins to exert their inhibitory effects.
Note that decreases in translation efficiency activate toxins Wood Page 9 Environ Microbiol. Author manuscript, available in PMC 2010 January 1. NIH PA Author Manuscript NIH PA Author Manuscript NIH PA Author Manuscript. Hha also activates the prophage genes rzpD, yfjZ, alpA, and appY which actively lyse cells. Hence, Hha is toxic indirectly by activating other toxins by changing translation efficiency. Therefore, one of the most important roles of the nebulous T AT pairs is to help control biofilm formation. Small RNA and biofilm dispersal Biofilm dispersal is important for disseminating the strain, however, for the bacterium to leave the solid matrix in which it is both protected and entrapped, it may be necessary to sacrifice part of the biofilm and have some cells undergo autolysis.
Hence, programmed cell death may make sense for the biofilm and the primitive tissue that this collection of cells represents but not for planktonic cells. Biofilm dispersal for P. aeruginosa involves prophage and in Pseudoalteromonas tunicata involves the autolytic protein AlpA. In E. coli, along with cell toxicity and biofilm formation, Hha appears to control biofilm dispersal. Initial evidence is that Hha leads to decreased biofilm in flow cells and to the formation of plaques, cell lysis via Hha may aid biofilm dispersal by forming holes
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