Number Of Environmental Signals Research Articles

GltS regulates biofilm formation in methicillin-resistant Staphylococcus aureus

Biofilm-based infection is a major healthcare burden. Methicillin-resistant Staphylococcus aureus (MRSA) is one of major organisms responsible for biofilm infection. Although biofilm is induced by a number of environmental signals, the molecule responsible for environmental sensing is not well delineated. Here we examined the role of ion transporters in biofilm formation and found that the sodium-glutamate transporter gltS played an important role in biofilm formation in MRSA. This was shown by gltS transposon mutant as well as its complementation. The lack of exogenous glutamate also enhanced biofilm formation in JE2 strain. The deficiency of exogenous glutamate intake accelerated endogenous glutamate/glutamine production, which led to the activation of the urea cycle. We also showed that urea cycle activation was critical for biofilm formation. In conclusion, we showed that gltS was a critical regulator of biofilm formation by controlling the intake of exogenous glutamate. An intervention to target glutamate intake may be a potential useful approach against biofilm.

Vibrio cholerae secretion system of the type VI

The review summarizes literature data on the Vibrio cholerae secretion system of the 6th type. This system is a contact-dependent macromolecular mechanism through which bacteria translocate toxic effector proteins into target cells. It is found in many Gram-negative bacteria, including Vibrio cholerae. V. cholerae infects phagocytic amoebae, nematodes, ciliates, bacteria belonging to different species, as well as unrelated strains of V. cholerae using this system. DNA released after lysis of competing bacteria can be taken up by Vibrio cholerae cells, which leads to the acquisition of new genetic material. The type VI secretion system is involved in the infectious process. The destruction of macrophages and microbiota contributes to the active reproduction of the pathogen and colonization of host epitheliocytes, and the production of effector proteins causes the development of diarrhea and intestinal inflammation. Cholera vibrio secretion system of the 6th type has a structure similar to other gram-negative bacteria. The genes encoding the proteins of this system are located in one large region of the second chromosome and in several additional clusters. It has been shown that toxigenic strains of V. cholerae contain an identical set of secretion system genes, while their composition is variable in non-toxigenic isolates. The regulation of secretion system protein expression differs in V. cholerae strains of different toxigenicity, depends on a number of environmental signals, and is associated with other cell regulatory networks. The paper provides experimental data on the analysis of the structure of the global regulatory gene, vasH, of the type VI secretion system in toxigenic and non-toxigenic V. cholerae O1, biovar El Tor strains isolated in the Russian Federation. Thus, the type VI secretion system is an important mechanism that facilitates the survival of V. cholerae in complex communities in vitro, protects against damaging factors of the macroorganism and increases virulence in vivo, and also provides evolutionary transformations of cholera vibrio. Further study of this system will allow a better understanding of the pathogen-host interaction processes, as well as the adaptation mechanisms of V. cholerae in the external environment.

Inducing broadcast coral spawning ex situ: Closed system mesocosm design and husbandry protocol.

For many corals, the timing of broadcast spawning correlates strongly with a number of environmental signals (seasonal temperature, lunar, and diel cycles). Robust experimental studies examining the role of these putative cues in triggering spawning have been lacking until recently because it has not been possible to predictably induce spawning in fully closed artificial mesocosms. Here, we present a closed system mesocosm aquarium design that utilizes microprocessor technology to accurately replicate environmental conditions, including photoperiod, seasonal insolation, lunar cycles, and seasonal temperature from Singapore and the Great Barrier Reef (GBR), Australia. Coupled with appropriate coral husbandry, these mesocosms were successful in inducing, for the first time, broadcast coral spawning in a fully closed artificial ex situ environment. Four Acropora species (A. hyacinthus, A. tenuis, A. millepora, and A. microclados) from two geographical locations, kept for over 1 year, completed full gametogenic cycles ex situ. The percentage of colonies developing oocytes varied from ~29% for A. hyacinthus to 100% for A. millepora and A. microclados. Within the Singapore mesocosm, A. hyacinthus exhibited the closest synchronization to wild spawning, with all four gravid colonies releasing gametes in the same lunar month as wild predicted dates. Spawning within the GBR mesocosm commenced at the predicted wild spawn date but extended over a period of 3 months. Gamete release in relation to the time postsunset for A. hyacinthus, A. millepora, and A. tenuis was consistent with time windows previously described in the wild. Spawn date in relation to full moon, however, was delayed in all species, possibly as a result of external light pollution. The system described here could broaden the number of institutions on a global scale, that can access material for broadcast coral spawning research, providing opportunities for institutions distant from coral reefs to produce large numbers of coral larvae and juveniles for research purposes and reef restoration efforts.

Stringent Response Regulation of Biofilm Formation in Vibrio cholerae

Biofilm formation is a key factor in Vibrio cholerae environmental survival and host colonization. Production of biofilm enables V. cholerae to survive and persist in aquatic environments and aids in the passage through the gastric acid barrier to allow access to the small intestine. The genes involved in biofilm formation are regulated by the transcriptional activators vpsR and vpsT, which are in turn transcriptionally regulated by a number of environmental signals. In this study, the role of the stringent response in biofilm formation was examined. V. cholerae mutants deficient in stringent response had a reduced ability to form biofilms, although they were not completely deficient in biofilm formation. There are three (p)ppGpp synthases in V. cholerae: RelA, SpoT, and RelV. All three synthases were necessary for vpsR transcription, with RelV showing the strongest effect. RelA was the only synthase that was necessary for vpsT expression. Stringent response regulation of vpsR and vpsT was shown to partially occur through rpoS. Biofilm formation in V. cholerae is controlled by a complex regulatory apparatus, with negative regulators of biofilm gene expression, such as quorum sensing, and positive regulators of biofilm genes, including stringent response, interacting to ensure that biofilm formation is coordinated with the environment.

Acceleration of Flowering during Shade Avoidance in Arabidopsis Alters the Balance betweenFLOWERING LOCUS C-Mediated Repression and Photoperiodic Induction of Flowering

The timing of the floral transition in Arabidopsis (Arabidopsis thaliana) is influenced by a number of environmental signals. Here, we have focused on acceleration of flowering in response to vegetative shade, a condition that is perceived as a decrease in the ratio of red to far-red radiation. We have investigated the contributions of several known flowering-time pathways to this acceleration. The vernalization pathway promotes flowering in response to extended cold via transcriptional repression of the floral inhibitor FLOWERING LOCUS C (FLC); we found that a low red to far-red ratio, unlike cold treatment, lessened the effects of FLC despite continued FLC expression. A low red to far-red ratio required the photoperiod-pathway genes GIGANTEA (GI) and CONSTANS (CO) to fully accelerate flowering in long days and did not promote flowering in short days. Together, these results suggest a model in which far-red enrichment can bypass FLC-mediated late flowering by shifting the balance between FLC-mediated repression and photoperiodic induction of flowering to favor the latter. The extent of this shift was dependent upon environmental parameters, such as the length of far-red exposure. At the molecular level, we found that far-red enrichment generated a phase delay in GI expression and enhanced CO expression and activity at both dawn and dusk. Finally, our analysis of the contribution of PHYTOCHROME AND FLOWERING TIME1 (PFT1) to shade-mediated rapid flowering has led us to suggest a new model for the involvement of PFT1 in light signaling.

Adhesin - receptor interactions in the attachment ofCandida albicansto host epithelial cells

The ability of Candida albicans to adhere to a variety of host surfaces is thought to be an important factor in the pathogenesis of candidosis. Adhesion of the yeast form of the fungus to epithelial cells can involve several kinds of adhesion – receptor interaction. Yeast adhesins are typically mannoproteins associated with fibrils or fimbriae on the fungal surface. Lectinlike interactions have been identified between the protein portion of two mannoprotein adhesins and glycosides containing L-fucose or N-acetylglucosamine. The fucoside-binding adhesin has been purified and shown to have an affinity for glycosphingolipid receptors carrying the H blood-group antigen. A fimbrial adhesin has also been described that binds to gangliosides containing a βGalNAc(1–4)βGal disaccharide sequence. Other mannoprotein adhesins proposed recently include the factor 6 epitope present on serotype A strains of C. albicans and an integrin analogue. Adhesin expression appears to be regulated by a number of environmental signals, including osmolarity and the availability of iron and sugars. Additional adhesion-dependent signals might trigger further responses such as the initiation of morphogenesis. Key words: Candida albicans, yeast adhesion, epithelial cell adhesion.