Gilesbest8772

Cyanobacteria are globally important primary producers and nitrogen fixers. They are frequently limited by iron bioavailability in natural environments that often fluctuate due to rapid consumption and irregular influx of external Fe. Here we identify a succession of physiological changes in Synechocystis sp. PCC 6803 occurring over 14-16 days of iron deprivation and subsequent recovery. We observe several adaptive strategies that allow cells to push their metabolic limits under the restriction of declining intracellular Fe quotas. Interestingly, cyanobacterial populations exposed to prolonged iron deprivation showed discernible heterogeneity in cellular auto-fluorescence during the recovery process. Using FACS and microscopy techniques we revealed that only cells with high auto-fluorescence were able to grow and reconstitute thylakoid membranes. We propose that ROS-mediated damage is likely to be associated with the emergence of the two subpopulations, and, indeed, a rapid increase in intracellular ROS content was observed during the first hours following iron addition to Fe-starved cultures. These results suggest that an increasing iron supply is a double-edged sword - posing both an opportunity and a risk. Therefore, phenotypic heterogeneity within populations is crucial for the survival and proliferation of organisms facing iron fluctuations within natural environments.l-rhamnose is found in nature mainly as a component of structural plant polysaccharides and can be used as a carbon source by certain microorganisms. Catabolism of this sugar in bacteria, archaea and fungi occurs by two routes involving either phosphorylated or non-phosphorylated intermediates. Unlike the corresponding pathway in yeasts, the metabolic details of the non-phosphorylated pathway in filamentous fungi are not fully defined. The first three genes (lraA, lraB and lraC) of the non-phosphorylated pathway in Aspergillus nidulans have recently been studied revealing dependence on lraA function for growth on l-rhamnose and α-l-rhamnosidase production. In the present work, two genes encoding the subsequent steps catalysed by l-2-keto-3-deoxyrhamnonate (l-KDR) aldolase (AN9425) and l-lactaldehyde dehydrogenase (AN0554) are identified. Loss-of-function mutations cause adverse growth effects on l-rhamnose. Akin to genes lraA-C and those encoding rhamnosidases (rhaA, rhaE), their expression is induced on l-rhamnose via the transcriptional activator RhaR. Interestingly, the aldolase belongs to the ftablamily of bacterial l-KDR aldolases (PF03328/COG3836) and not that of yeasts (PF00701/COG0329). In addition, AN0554 corresponds to the previously characterized aldA gene (encodes aldehyde dehydrogenase involved in ethanol utilization) thus revealing a previously unknown role for this gene in the catabolism of l-rhamnose.Paenibacillus larvae is the causative agent of the fatal American foulbrood disease in honeybees (Apis mellifera). Strain identification is vital for preventing the spread of the disease. To date, the most accessible and robust scheme to identify strains is the multilocus sequence typing (MLST) method. However, this approach has limited resolution, especially for epidemiological studies. As the cost of whole-genome sequencing has decreased and as it becomes increasingly available to most laboratories, an extended MLST based on the core genome (cgMLST) presents a valuable tool for high-resolution investigations. In this study, we present a standardized, robust cgMLST scheme for P. larvae typing using whole-genome sequencing. A total of 333 genomes were used to identify, validate and evaluate 2419 core genes. The cgMLST allowed fine-scale differentiation between samples that had the same profile using traditional MLST and allowed for the characterization of strains impossible by MLST. The scheme was successfully used to trace a localized Swedish outbreak, where a cluster of 38 isolates was linked to a country-wide beekeeping operation. cgMLST greatly enhances the power of a traditional typing scheme, while preserving the same stability and standardization for sharing results and methods across different laboratories.The cell membrane glycoprotein CD26 with peptidase activity (DPP4) and/or its soluble CD26/DPP4 counterpart expression and/or activity are altered in several cancers. Its role in metastasis development was recently highlighted by the discovery of CD26+ cancer stem cell subsets and the fact that clinical DPP4 inhibitors showed antimetastatic effects in animal models. Also, diabetic patients treated with the DPP4 inhibitor sitagliptin showed greater overall survival after colorectal or lung cancer surgery than patients under other diabetic therapies. However, the mechanism of action of these inhibitors in this context is unclear. We studied the role of CD26 and its DPP4 enzymatic activity in malignant cell features such as cell-to-cell homotypic aggregation, cancer cell motility, and invasion in a panel of human colorectal cancer (CRC) cell lines, avoiding models that include the physiological role of DPP4 in chemotaxis. Present results indicate that CD26 participates in the induction of cell invasion, motility, and aggregation of CD26-positive CRC cell lines. this website Moreover, only invasion and motility assays, which are collagen matrix-dependent, showed a decrease upon treatment with the DPP4 inhibitor sitagliptin. Sitagliptin showed opposite effects to those of transforming growth factor-β1 on epithelial-to-mesenchymal transition and cell cycle, but this result does not explain its CD26/DPP4-dependent effect. These results contribute to the elucidation of the molecular mechanisms behind sitagliptin inhibition of metastatic traits. At the same time, this role of sitagliptin may help to define areas of medicine where DPP4 inhibitors might be introduced. However, they also suggest that additional tools against CD26 as a target might be used or developed for metastasis prevention in addition to gliptins.Interkingdom communication is of particular relevance in polymicrobial biofilms. In this work, the ability of the fungus Ophiostoma piceae to form biofilms individually and in consortium with the bacterium Pseudomonas putida, as well as the effect of fungal and bacterial signal molecules on the architecture of the biofilms was evaluated. Pseudomonas putida KT2440 is able to form biofilms through the secretion of exopolysaccharides and two large extracellular adhesion proteins, LapA and LapF. It has two intercellular signalling systems, one mediated by dodecanoic acid and an orphan LuxR receptor that could participate in the response to AHL-type quorum sensing molecules (QSMs). Furthermore, the dimorphic fungus O. piceae uses farnesol as QSM to control its yeast to hyphae morphological transition. Results show for the first time the ability of this fungus to form biofilms alone and in mixed cultures with the bacterium. Biofilms were induced by bacterial and fungal QSMs. The essential role of LapA-LapF proteins in the architecture of biofilms was corroborated, LapA was induced by farnesol and dodecanol, while LapF by 3-oxo-C6-HSL and 3-oxo-C12-HSL.