Chemotaxis and haptotaxis are important biological mechanisms that influence microbial movement toward concentrated chemoattractants in mobile liquids and along immobile surfaces, respectively. This study investigated their coupled effect, as induced by naphthalene (10 mg L-1), on the transport and retention of two pollutant-degrading bacteria, Pseudomonas fluorescens 5RL (Pf5RL) and Pseudomonas stutzeri DQ1 (PsDQ1), in quartz sand and natural soil. The results demonstrated that PsDQ1 was not chemotactic, whereas Pf5RL was chemotactic at 25°C but not at 4°C due to the restricted movement. https://www.selleckchem.com/products/tuvusertib.html In a quartz sand column, haptotaxis did not play a role in increasing the transport of Pf5RL as compared with chemotaxis. Compared with a naphthalene-free soil column, Pf5RL broke through naphthalene-presaturated soil columns to reach a stable effluent concentration 0.5 pore volumes earlier due to advective chemotaxis occurring behind the plume front in the bulk solution. Pf5RL also demonstrated greater retention (e.g., a doubled rate of attachment and a one-third smaller breakthrough percentage) due to along-surface haptotaxis and near-surface chemotaxis occurring in less mobile water near the soil surface. However, both chemotaxis and haptotaxis were weakened when Pf5RL co-transported with naphthalene due to reduced adsorption of naphthalene on the soil. This study suggests that surface adsorption of naphthalene can mediate the relative importance of advective chemotaxis (facilitating initial breakthrough), near-surface chemotaxis (increasing bacterial collision), and haptotaxis (increasing bacterial residence time). Copyright © 2019 Yang, Chen, Zeng, Radosevich, Ripp, Zhuang and Sayler.Autophagy is mainly a catabolic process, which is used to cope with nutrient deficiency and various stress conditions. Human environment often imposes various stresses on Cryptococcus neoformans, a major fungal pathogen of immunocompromised individuals; therefore, autophagic response of C. neoformans to these stresses often determines its survival in the host. However, a systematic study on how autophagy related (ATG) genes influence on autophagic flux, virulence, stress response and pathogenicity of C. neoformans is lacking. In this study, 22 ATG-deficient strains were constructed to investigate their roles in virulence, pathogenesis, stress response, starvation tolerance and autophagic flux in C. neoformans. Our results showed that Atg6 and Atg14-03 significantly affect the growth of C. neoformans at 37°C and laccase production. Additionally, atg2Δ and atg6Δ strains were sensitive to oxidative stress caused by hydrogen peroxide. Approximately half of the atgΔ strains displayed higher sensitivity to 1.5 M NaCl and remarkably lower virulence in the Galleria mellonella model than the wild type. Autophagic flux in C. neoformans was dependent on the Atg1-Atg13, Atg5-Atg12-Atg16, and Atg2-Atg18 complexes and Atg11. Cleavage of the green fluorescent protein (GFP) from Atg8 was difficult to detect in these autophagy defective mutants; however, it was detected in the atg3Δ, atg4Δ, atg6Δ and atg14Δ strains. Additionally, no homologs of Saccharomyces cerevisiae ATG10 were detected in C. neoformans. Our results indicate that these ATG genes contribute differentially to carbon and nitrogen starvation tolerance in C. neoformans compared with S. cerevisiae. Overall, this study advances our knowledge of the specific roles of ATG genes in C. neoformans. Copyright © 2019 Zhao, Feng, Zhu, Li, Ma, Li, Zhu and Wei.A hallmark of inflammatory responses is leukocyte mobilization, which is mediated by pathogen and host released chemotactic factors that activate Gi-protein-coupled seven-transmembrane receptors (GPCRs) on host cell surface. Formylpeptide receptors (FPRs, Fprs in mice) are members of the chemoattractant GPCR family, shown to be critical in myeloid cell trafficking during infection, inflammation, immune responses, and cancer progression. Accumulating evidence demonstrates that both human FPRs and murine Fprs are involved in a number of patho-physiological processes because of their expression on a wide variety of cell types in addition to myeloid cells. The unique capacity of FPRs (Fprs) to interact with numerous structurally unrelated chemotactic ligands enables these receptors to participate in orchestrated disease initiation, progression, and resolution. One murine Fpr member, Fpr2, and its endogenous agonist peptide, Cathelicidin-related antimicrobial peptide (CRAMP), have been demonstrated as key mediators of colon mucosal homeostasis and protection from inflammation and associated tumorigenesis. Recent availability of genetically engineered mouse models greatly expanded the understanding of the role of FPRs (Fprs) in pathophysiology that places these molecules in the list of potential targets for therapeutic intervention of diseases. Copyright © 2020 Liang, Chen, Gong, Yoshimura, Le, Wang and Wang.Objective To clarify the role and mechanism of miR-17-92 cluster in islet beta-cell repair after streptozotocin intervention. Methods Genetically engineered mice (miR-17-92βKO) and control RIP-Cre mice were intraperitoneally injected with multiple low dose streptozotocin. Body weight, random blood glucose (RBG), fasting blood glucose, and intraperitoneal glucose tolerance test (IPGTT) were monitored regularly. Mice were sacrificed for histological analysis 8 weeks later. Morphological changes of pancreas islets, quantity, quality, apoptosis, and proliferation of beta-cells were measured. Islets from four groups were isolated. MiRNA and mRNA were extracted and quantified. Results MiR-17-92βKO mice showed dramatically elevated fasting blood glucose and impaired glucose tolerance after streptozotocin treatment in contrast to control mice, the reason of which is reduced beta-cell number and total mass resulting from reduced proliferation, enhanced apoptosis of beta-cells. Genes related to cell proliferation and insulin transcription repression were significantly elevated in miR-17-92βKO mice treated with streptozotocin. Furthermore, genes involved in DNA biosynthesis and damage repair were dramatically increased in miR-17-92βKO mice with streptozotocin treatment. Conclusion Collectively, our results demonstrate that homozygous deletion of miR-17-92 cluster in mouse pancreatic beta-cells promotes the development of experimental diabetes, indicating that miR-17-92 cluster may be positively related to beta-cells restoration and adaptation after streptozotocin-induced damage. Copyright © 2020 Wan, Zhang, Chen, Lang, Li, Chen, Tian, Meng and Yu.