Synthetic analogs of rhamnolipids modulate structured biofilms formed by rhamnolipid-nonproducing mutant of Pseudomonas aeruginosa.

Rhamnolipids secreted by Pseudomonas aeruginosa are required for the bacteria to form biofilm efficiently and form biofilm with internal structures including pores and channels. In this work, we explore the effect of a class of synthetic analogs of rhamnolipids at controlling (promoting and inhibiting) the biofilm formation activities of a non-rhamnolipid-producing strain - rhlA - of P. aeruginosa. This class of rhamnolipid analogs is known to modulate the swarming motilities of wild-type PAO1 and rhlA mutant, but its effect on biofilm formation of rhlA mutant is unknown. We show that small structural details of these molecules are important for the bioactivities, but do not affect the general physical properties of the molecules. The bioactive synthetic analogs of rhamnolipids promote biofilm formation by rhlA mutant at low concentrations, but inhibit the biofilm formation at high concentrations. To explore the internal structures formed by the biofilms, we first demonstrate that wild-type biofilms are formed with substantial topography (hills and valleys) when the sample is under shaking conditions. Using this observation as a comparison, we found that synthetic analogs of rhamnolipids promoted structured (porous) biofilm of rhlA mutant, at intermediate concentrations between the low ones that promoted biofilm formation and the high ones that inhibited biofilm formation. This study suggests a potential chemical signaling approach to control multiple bacterial activities.

Chemical Signals of Synthetic Disaccharide Derivatives Dominate Rhamnolipids at Controlling Multiple Bacterial Activities.

Microbes secrete molecules that modify their environment. Here, we demonstrate a class of synthetic disaccharide derivatives (DSDs) that mimics and dominates the activity of naturally secreted rhamnolipids by Pseudomonas aeruginosa. The DSDs exhibit the dual function of activating and inhibiting the swarming motility through a concentration-dependent activity reversal that is characteristic of signaling molecules. Whereas DSDs tethered with a saturated farnesyl group exhibit inhibition of both biofilm formation and swarming motility, with higher activities than rhamnolipids, a saturated farnesyl tethered with a sulfonate group only inhibits swarming motility but promote biofilm formation. These results identified important structural elements for controlling swarming motility, biofilm formation, and bacterial adhesion and suggest an effective chemical approach to control intertwined signaling processes that are important for biofilm formation and motilities.

Specific maltose derivatives modulate the swarming motility of nonswarming mutant and inhibit bacterial adhesion and biofilm formation by Pseudomonas aeruginosa.

We have demonstrated that specific synthetic maltose derivatives activate the swarming motility of a Pseudomonas aeruginosa nonswarming mutant (rhlA) at low concentration, but inhibit it at high concentration. Although these molecules are not microbicidal, active maltose derivatives with bulky hydrocarbon groups inhibited bacterial adhesion, and exhibited biofilm inhibition and dispersion (IC50 ~20 µM and DC50 ~30 µM, respectively). Because the swarming motility of the rhlA mutant is abolished by the lack natural rhamnolipids, the swarming activation suggests that maltose derivatives are analogues of rhamnolipids. Together, these results suggest a new approach of controlling multiple bacterial activities (bacterial adhesion, biofilm formation, and swarming motility) by a set of disaccharide-based molecules.

Expression profile of myostatin mRNA during the embryonic organogenesis of domestic chicken (Gallus gallus domesticus).

Myostatin is a potent growth and differentiation factor involved in skeletal muscle tissue formation in vertebrates. However, recent studies in chicken embryo suggested that the myostatin was expressed even before the establishment of myogenic lineage. No studies have thus far been reported in birds to define the role of myostatin during the embryonic organogenesis. The present experiment was designed for studying the expression profiles of myostatin mRNA in the chicken liver, heart, brain, and intestine during their morphogenesis, using real-time PCR. The myostatin mRNA expression was significantly upregulated in liver during E15-E18. Similar results were observed during the development of chicken heart. In brain, the expression of myostatin was upregulated from E4 onwards. In intestine, the expression of myostatin was significantly increased many folds on E9-E18. Therefore, the increase in myostatin expression might be related to the growth of liver and heart on days E12-E18; morphogenesis and growth of brain during E15-E18; and morphogenesis and differentiation of intestine during E9-E18. In the present study, the tissue-specific expression of myostatin gene in chicken is similar to fishes, but different from that in mammals. Further, the inspection of chicken genome also suggested that there is no differentiation of GDF-8 and -11. A recent finding suggests that the chicken myostatin gene is closely related to mammals than fishes. Therefore, we propose that the chicken myostatin gene might have diverged in its function between teleosts and mammals. Indeed it is possible that its function might have only become fully differentiated to serve as a control of muscle mass in mammals.