Browsing tag: transformacja

Mikrobiologiczne przemiany kwasu wanilinowego

Microbial transformation of vanillic acid
M. Kurek, I. Greń

1. Wprowadzenie. 2. Mikrobiologiczny rozkład kwasu wanilinowego. 2.1. Demetylacja kwasu wanilinowego. 2.2. Dekarboksylacja kwasu wanilinowego. 2.3. Redukcja kwasu wanilinowego. 3. Synteza kwasu wanilinowego. 3.1. Synteza kwasu wanilinowego z kwasu ferulowego. 3.2. Synteza kwasu wanilinowego z eugenolu i izoeugenolu. 4. Podsumowanie

Abstract: Increasing demand for natural vanillic aroma in food industry as well as law restrictions for the usage of chemically synthesized compounds in natural fragrances caused large interest in vanillic production via biotechnological processes. Because vanillic acid is the main substrate for vanillic production, the knowledge of biological processes of its synthesis and the release from lignin is crucial for developing the optimal biotechnological processes. Some microorganisms are able to synthesize vanillic acid form naturally occurring compounds, such as ferulic acid, eugenol and isoeugenol using biotransformation reactions. Large amount of vanillin are produced by reduction of vanillic acid by carboxylic acid reductase (Car). Another pathways of vanillic acid transformation are based on its demethylation and decarboxylaction reactions. O-demethylases are NAH(P)H or tetrahydrofolic dependent enzymes. This review presents short characterization of vanillic acid transformation processes by microorganisms.

1. Introduction. 2. Microbial degradation of vanillic acid. 2.1. Demetylation of vanillic acid. 2.2. Decarboxylation of vanillic acid. 2.3. Reduction of vanillic acid. 3. Synthesis of vanillic acid. 3.1. Synthesis of vanillic acid from ferulic acid. 3.2. Synthesis of vanillic acid from eugenol and isoeugenol. 4. Summary

Plastyczność bakteryjnych genomów – międzykomórkowy transfer informacji genetycznej

Bacterial genome plasticity – intercellular transfer of genetic information
U. Kasprzykowska, B. M. Sobieszczańska

1. Wstęp. 2. Transdukcja – bakteriofagi. 3. Koniugacja i plazmidy. 4. Transformacja. 5. Podsumowanie

Abstract: Mutations in the bacterial genomes are responsible for minor genetic changes. Most extensive restructuring of bacterial genomes arise from inter- and intragenetic gene transfer. Multiple types of transposition elements responsible for movement of DNA within cells have been described. All these transposable elements may outreach other cells of the same bacterial species or bacteria of another species via transduction, conjugation and transformation. These three mechanisms of horizontal gene transfer have a great impact on evolution of prokaryotic organisms by allowing molecular innovations to spread among bacteria and promote their adaptation to a new environments. On the other hand, horizontal gene transfer also enables bacteria to adapt to the host both, by spreading virulence determinants and allowing pathogens to acquire genes of resistance to many antimicrobials. This review presents phenomenons of transduction, conjugation and transformation, as three distinct mechanisms of intercellular DNA transfer that provide potential evolutionary advantage to prokaryotes.

1. Introduction. 2. Transduction – bacteriophages. 3. Conjugation and plasmids. 4. Transformation. 5.Summary.

Sekrecja pęcherzyków błonowych jako mechanizm promujący infekcje H. pylori

Secretion of outer membrane vesicles as a mechanism promoting H. pylori infections
P. Krzyżek

1. Wstęp. 2. Sekrecja pęcherzyków błonowych u H. pylori. 3. Proteom pęcherzyków błonowych H. pylori. 4. Transport czynników wirulencji poprzez OMV. 4.1. Toksyna VacA. 4.2. Onkoproteina CagA. 4.3. Inne substancje. 5. Udział OMV w formowaniu biofilmu. 5.1. Funkcje biofilmu. 5.2. Zaangażowanie OMV w tworzenie biofilmu u bakterii. 5.3. Zaangażowanie OMV w tworzenie biofilmu u H. pylori. 5.4. Funkcja strukturalna zewnątrzkomórkowego DNA H. pylori. 6. Zewnątrzkomórkowe DNA jako nośnik informacji. 6.1. Wpływ na wirulencję. 6.2. Transformacja. 6.3. Naturalna kompetencja H. pylori. 7. Podsumowanie

Abstract: Helicobacter pylori commonly colonizes the human gastric mucosa. Infections with this microorganism can contribute to serious health consequences, such as peptic ulceration, gastric adenocarcinoma and gastric mucosa-associated lymphoid tissue lymphoma. Chronic persistence of this bacteria in the host organism is probably strongly dependent on the secretion of outer membrane vesicles (OMV). These organelles are small, electron-dense, extracellular structures which are secreted in large amounts during stressful conditions, among others. H. pylori OMV mediate transfer of virulence factors such as toxins and immunomodulatory compounds. They contribute to avoiding a response from the host immune system and inducing chronic gastritis. OMV secretion also affects the formation of cell aggregates, microcolonies and biofilm matrix. Enhanced OMV production is connected to maintenance of direct contact through cell-cell and
cell-surface interactions. A key component of OMV, which determines their structural function, is extracellular DNA (eDNA) anchored to the surface of these organelles. eDNA associated with OMV additionally determines the genetic recombination in the process of horizontal gene transfer. H. pylori is naturally competent for genetic transformation and is constantly capable of DNA uptake from the environment. The natural competence state promotes the assimilation of eDNA anchored to the OMV surface. This is probably dependent on ComB and ComEC components, which are involved in the transformation process. For this reason, the OMV secretion mediates intensive exchange of genetic material, promotes adaptation to changing environmental conditions and enables persistent infecting of the gastric mucosa by H. pylori.

1. Introduction. 2. Secretion of outer membrane vesicles by H. pylori. 3. Proteome of H. pylori outer membrane vesicles. 4. Transport of virulence factors through OMV. 4.1. Toxin VacA. 4.2. Oncoprotein CagA. 4.3. Other substances. 5. OMV involvement in biofilm formation. 5.1. Functions of biofilm. 5.2. OMV influence on bacterial biofilm formation. 5.3. OMV influence on biofilm formation by H. pylori. 5.4. Structural function of H. pylori extracellular DNA. 6. Extracellular DNA as an information carrier. 6.1. Influence on virulence. 6.2. Transformation. 6.3. Natural competence of H. pylori. 7. Conclusions