The phylogenetic resolution at which microorganisms display geographic endemism, the rates at which they disperse at global scales, and the role of humans on global microbial dispersal are largely unknown. Answering these questions is necessary for interpreting microbial biogeography, ecology, and macroevolution and for predicting the spread of emerging pathogenic strains. To resolve these questions, I analyzed the geographic and evolutionary relationships between 36,795 bacterial and archaeal ("prokaryotic") genomes from ∼7000 locations around the world. I find clear signs of continental-scale endemism, including strong correlations between phylogenetic divergence and geographic distance. However, the phylogenetic scale at which endemism generally occurs is extremely small, and most "species" (defined by an average nucleotide identity ≥ 95%) and even closely related strains (average nucleotide identity ≥ 99.9%) are globally distributed. Human-associated lineages display faster dispersal rates than other terrestrial lineages; the average net distance between any two human-associated cell lineages diverging 50 years ago is roughly 580 km. These results suggest that many previously reported global-scale microbial biogeographical patterns are likely the result of recent or current environmental filtering rather than geographic endemism. For human-associated lineages, estimated transition rates between Europe and North America are particularly high, and much higher than for non-human associated terrestrial lineages, highlighting the role that human movement plays in global microbial dispersal. Dispersal was slowest for hot spring- and terrestrial subsurface-associated lineages, indicating that these environments may act as "isolated islands" of microbial evolution.The capability to respond to wounding is a process shared by organisms of different kingdoms that can result in the regeneration of whole-body parts or lost structures or organs. Filamentous fungi constitute a rich food source that ensures survival and reproduction of their predators and are therefore continuously exposed to mechanical damage. Nevertheless, our understanding of how fungi respond to wounding and predators is scarce. Fungi like plants and animals respond to injury recognizing Damage- and Microbe-Associated Molecular Patterns (DAMPs/MAMPs) that activate Ca2+ and Mitogen-Activated Protein Kinase dependent signaling for the activation of defense mechanisms. https://www.selleckchem.com/products/epacadostat-incb024360.html During herbivory, plants, in addition to activating pathways related to injury, activate specific responses to combat their predators. Using a transcriptional approach, we studied the capacity of the filamentous fungus Trichoderma atroviride to activate specific responses to injury and attack by different arthropods. Attack by Drosophila melanogaster inhibited the transcriptional activation of genes required for hyphal regeneration, and the fungal innate immune and chemical defense responses. We also provide mechanistic insight of this inhibition involving components of the D. melanogaster salivary glands that repress the expression of a set of genes and block hyphal regeneration.The host range of parasites is an important factor in assessing the dynamics of disease epidemics. The evolution of pathogens to accommodate new hosts may lead to host range expansion, a process the molecular bases of which are largely enigmatic. The fungus Sclerotinia sclerotiorum has been reported to parasitize more than 400 plant species from diverse eudicot families while its close relative, S. trifoliorum, is restricted to plants from the Fabaceae family. We analyzed S. sclerotiorum global transcriptome reprogramming on hosts from six botanical families and reveal a flexible, host-specific transcriptional program. We generated a chromosome-level genome assembly for S. trifoliorum and found near-complete gene space conservation in two representative strains of broad and narrow host range Sclerotinia species. However, S. trifoliorum showed increased sensitivity to the Brassicaceae defense compound camalexin. Comparative analyses revealed a lack of transcriptional response to camalexin in the S. trifoliorum strain and suggest that regulatory variation in detoxification and effector genes at the population level may associate with the genetic accommodation of Brassicaceae in the Sclerotinia host range. Our work proposes transcriptional plasticity and the co-existence of signatures for generalist and polyspecialist adaptive strategies in the genome of a plant pathogen.Synovial hyperplasia, a profound alteration in the structure of synovial tissue, is the basis for cumulative joint destruction in rheumatoid arthritis (RA). It is generally accepted that controlling synovial hyperplasia can delay the progression of RA. As one of the most intensively studied isoforms of acid-sensing ion channels (ASICs), ASIC1a contributes to various physiopathologic conditions, including RA, due to its unique property of being permeable to Ca2+. However, the role and the regulatory mechanisms of ASIC1a in synovial hyperplasia are poorly understood. Here, rats induced with adjuvant arthritis (AA) and human primary synovial fibroblasts were used in vivo and in vitro to investigate the role of ASIC1a in the proliferation of RA synovial fibroblasts (RASFs). The results show that the expression of ASIC1a was significantly increased in synovial tissues and RASFs obtained from patients with RA as well as in the synovium of rats with AA. Moreover, extracellular acidification improved the ability of RASFs colony formation and increased the expression of proliferation cell nuclear antigen (PCNA) and Ki67, which was abrogated by the specific ASIC1a inhibitor psalmotoxin-1 (PcTX-1) or ASIC1a-short hairpin RNA (ASIC1a-shRNA), suggesting that extracellular acidification promotes the proliferation of RASFs by activating ASIC1a. In addition, the activation of c-Raf and extracellular signal-regulated protein kinases (ERKs) signaling was blocked with PcTX-1 or ASIC1a-shRNA and the proliferation of RASFs was further inhibited by the ERK inhibitor (U0126), indicating that ERK/MAPK signaling contributes to the proliferation process of RASFs promoted by the activation of ASIC1a. These findings gave us an insight into the role of ASIC1a in the proliferation of RASFs, which may provide solid foundation for ASIC1a as a potential target in the treatment of RA.


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Last-modified: 2025-01-23 (木) 05:25:42 (26d)