Effects of altered river network connectivity on the distribution of Salmo trutta: Insights from a metapopulation model

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A Virulent Phage Infecting Lactococcus garvieae,with Homology to Lactococcus lactis Phages

A new virulent phage belonging to the Siphoviridae family and able to infect Lactococcus garvieae strains was isolated from compost soil. Phage GE1 has a prolate capsid (56 by 38 nm) and a long noncontractile tail (123 nm). It had a burst size of 139 and a latent period of 31 min. Its host range was limited to only two L. garvieae strains out of 73 tested. Phage GE1 has a double-stranded DNA genome of 24,847 bp containing 48 predicted open reading frames (ORFs). Putative functions could be assigned to only 14 ORFs, and significant matches in public databases were found for only 17 ORFs, indicating that GE1 is a novel phage and its genome contains several new viral genes and encodes several new viral proteins. Of these 17 ORFs, 16 were homologous to deduced proteins of virulent phages infecting the dairy bacterium Lactococcus lactis, including previously characterized prolate-headed phages. Comparative genome analysis confirmed the relatedness of L. garvieae phage GE1 to L. lactis phages c2 (22,172 bp) and Q54 (26,537 bp), although its genome organization was closer to that of phage c2. Phage GE1 did not infect any of the 58 L. lactis strains tested. This study suggests that phages infecting different lactococcal species may have a common ancestor.     

Suppression of Dwarf and irregular xylem Phenotypes Generates Low-Acetylated Biomass Lines in Arabidopsis

eskimo1-5 (esk1-5) is a dwarf Arabidopsis (Arabidopsis thaliana) mutant that has a constitutive drought syndrome and collapsed xylem vessels, along with low acetylation levels in xylan and mannan. ESK1 has xylan O-acetyltransferase activity in vitro. We used a suppressor strategy on esk1-5 to screen for variants with wild-type growth and low acetylation levels, a favorable combination for ethanol production. We found a recessive mutation in the KAKTUS (KAK) gene that suppressed dwarfism and the collapsed xylem character, the cause of decreased hydraulic conductivity in the esk1-5 mutant. Backcrosses between esk1-5 and two independent knockout kak mutants confirmed suppression of the esk1-5 effect. kak single mutants showed larger stem diameters than the wild type. The KAK promoter fused with a reporter gene showed activity in the vascular cambium, phloem, and primary xylem in the stem and hypocotyl. However, suppression of the collapsed xylem phenotype in esk1 kak double mutants was not associated with the recovery of cell wall O-acetylation or any major cell wall modifications. Therefore, our results indicate that, in addition to its described activity as a repressor of endoreduplication, KAK may play a role in vascular development. Furthermore, orthologous esk1 kak double mutants may hold promise for ethanol production in crop plants.Today, the fields of agriculture and forestry must address challenging issues, particularly in the context of fluctuating environmental conditions, such as ensuring that food and feed production remain efficient, meeting societal demands to reduce inputs, including water, and creating new products, such as biofuel. The demand for biofuel, a renewable alternative to fossil fuel, further increases the need to develop biomass amenable to alcohol fermentation. Second-generation biofuels are based on the fermentation of sugars extracted from lignocellulosic biomass, which is produced from the residues of food crops or from nonfood crops; therefore, its production does not compete with food crops (Sims et al., 2010). This lignocellulosic biomass is made up of secondary cell walls, mostly found in vascular tissues.Vascular tissues consist of a network of conduits, spanning an entire plant and connecting biosynthetically active leaves to the soil via the root and the shoot. There are two main vascular tissues, the xylem and the phloem, which arise from a lateral meristem called the procambium during primary growth. When dicot plants undergo secondary growth and cell walls are thickening, a secondary meristem, called the cambium or vascular cambium, emerges, giving rise to secondary vascular tissues (Esau, 1965; Buvat, 1989). The xylem is responsible for the upward transport of water and nutrients from the soil to the whole plant. The phloem, positioned parallel to the xylem, supplies sink organs (roots, etc.) with leaf photoassimilates. In angiosperms, such as Arabidopsis (Arabidopsis thaliana), the xylem is composed of two main cellular types, tracheary elements, involved in the transport of water, and fibers, playing a major role in plant support (Turner and Sieburth, 2003). The function of the xylem depends on the plant’s capacity to form thick secondary cell walls that confer mechanical strength to resist gravity and withstand negative pressure, allowing sap to travel upward through vessels. Xylem tissue is a major carbon sink that incorporates sugars into biopolymers (Ragni et al., 2011). Xylem secondary cell walls are mainly composed of cellulose embedded in a matrix of lignin and hemicelluloses. Xylan is a major hemicellulose in monocot and dicot secondary cell walls (Faik, 2010). Xylan has a linear backbone of β-(1,4)-linked d-Xyl residues that can be mono- or di-O-acetylated at positions O-2 and O-3 of the xylosyl residues (Ebringerova and Heinze, 2000).O-Acetylation of polysaccharides reportedly has a negative effect on the utilization of lignocellulose, such as in the production of paper and bioethanol (Biely, 1985; Grohmann et al., 1989). A major xylan acetyltransferase was recently identified in Arabidopsis: TRICHOME BIREFRINGENCE-LIKE29/ESKIMO1 (TBL29/ESK1; Urbanowicz et al., 2014). esk1 knockout mutants show a 60% reduction in xylan acetylation and a lesser reduction in mannan acetylation (Xiong et al., 2013; Yuan et al., 2013). esk1 has been described previously as a genotype with drought stress symptoms (Bouchabke-Coussa et al., 2008; Lugan et al., 2009); its collapsed xylem vessels (irregular xylem [irx] phenotype) are assumed to be the cause of the drastic hydraulic conductivity drop, and thus the drought stress syndrome, including dwarfism (Lefebvre et al., 2011).To identify new mutations that restore plant stature but maintain a low xylan O-acetylation level, we explored the possibility of producing this combination by screening an esk1-5 ethyl methanesulfonate (EMS)-mutagenized population for nondwarf phenotypes. The suppressors of esk1 were called beem, for biomass enhancement in esk1-5 mutation background. Here, we describe the identification of one BEEM gene as KAKTUS/UBIQUITIN PROTEIN LIGASE3 (KAK/UPL3), which encodes a protein belonging to the E3-ubiquitin protein ligase family (Downes et al., 2003).     

Borrelia burgdorferi Promotes the Establishment of Babesia microti in the Northeastern United States

Babesia microti and Borrelia burgdorferi, the respective causative agents of human babesiosis and Lyme disease, are maintained in their enzootic cycles by the blacklegged tick (Ixodes scapularis) and use the white-footed mouse (Peromyscus leucopus) as primary reservoir host. The geographic range of both pathogens has expanded in the United States, but the spread of babesiosis has lagged behind that of Lyme disease. Several studies have estimated the basic reproduction number (R ₀) for B. microti to be below the threshold for persistence (<1), a finding that is inconsistent with the persistence and geographic expansion of this pathogen. We tested the hypothesis that host coinfection with B. burgdorferi increases the likelihood of B. microti transmission and establishment in new areas. We fed I. scapularis larva on P. leucopus mice that had been infected in the laboratory with B. microti and/or B. burgdorferi. We observed that coinfection in mice increases the frequency of B. microti infected ticks. To identify the ecological variables that would increase the probability of B. microti establishment in the field, we integrated our laboratory data with field data on tick burden and feeding activity in an R ₀ model. Our model predicts that high prevalence of B. burgdorferi infected mice lowers the ecological threshold for B. microti establishment, especially at sites where larval burden on P. leucopus is lower and where larvae feed simultaneously or soon after nymphs infect mice, when most of the transmission enhancement due to coinfection occurs. Our studies suggest that B. burgdorferi contributes to the emergence and expansion of B. microti and provides a model to predict the ecological factors that are sufficient for emergence of B. microti in the wild.     

Effects of daytime food intake on memory consolidation during sleep or sleep deprivation

Sleep enhances memory consolidation. Bearing in mind that food intake produces many metabolic signals that can influence memory processing in humans (e.g., insulin), the present study addressed the question as to whether the enhancing effect of sleep on memory consolidation is affected by the amount of energy consumed during the preceding daytime. Compared to sleep, nocturnal wakefulness has been shown to impair memory consolidation in humans. Thus, a second question was to examine whether the impaired memory consolidation associated with sleep deprivation (SD) could be compensated by increased daytime energy consumption. To these aims, 14 healthy normal-weight men learned a finger tapping sequence (procedural memory) and a list of semantically associated word pairs (declarative memory). After the learning period, standardized meals were administered, equaling either ～50% or ～150% of the estimated daily energy expenditure. In the morning, after sleep or wakefulness, memory consolidation was tested. Plasma glucose was measured both before learning and retrieval. Polysomnographic sleep recordings were performed by electroencephalography (EEG). Independent of energy intake, subjects recalled significantly more word pairs after sleep than they did after SD. When subjects stayed awake and received an energy oversupply, the number of correctly recalled finger sequences was equal to those seen after sleep. Plasma glucose did not differ among conditions, and sleep time in the sleep conditions was not influenced by the energy intake interventions. These data indicate that the daytime energy intake level affects neither sleep's capacity to boost the consolidation of declarative and procedural memories, nor sleep's quality. However, high energy intake was followed by an improved procedural but not declarative memory consolidation under conditions of SD. This suggests that the formation of procedural memory is not only triggered by sleep but is also sensitive to the fluctuations in the energy state of the body.     

The human MSH5 (MutS Homolog 5) protein localizes to mitochondria and protects the mitochondrial genome from oxidative damage

MutS homologs play a central role in maintaining genetic stability. We show that MSH5 (MutS Homolog 5) is localized into the mitochondria of germ and somatic cells. This protein binds to mtDNA and interacts with the Twinkle helicase and the DNA polymerase gamma. hMSH5 stimulates mtDNA repair in response to DNA damage induced by oxidative stress. Furthermore, we observed a subsarcolemmal accumulation of hMSH5 in COX negative muscle fibers of patients presenting a mitochondrial myopathy. We report a novel localization for hMSH5 suggesting that this protein may have functions other than those known in meiotic recombination.     

Atypical femoral fracture in a metastatic bone disease patient six months after discontinuation of denosumab received sequentially to previous bisphosphonate therapy - A case report

Although, both bisphosphonates and denosumab are effective in reducing the risk of skeletal-related events in patients with metastatic bone disease, many concerns were being raised about the possible association between their use and atypical femoral fractures. A case of an atypical femoral fracture in a metastatic bone disease patient, six months after discontinuation of long-term zoledronic acid therapy and sequential treatment with denosumab is reported. After extensive laboratory and imaging examination, the fracture was classified as atypical and it was finally treated with discontinuation of denosumab, long cephalomedullary interlocking nailing and vitamin D administration. Sequential treatment with bisphosphonates and denosumab in patients with metastatic bone disease, may lead to an overlapping treatment effect, increasing bone suppression and the risk of atypical femoral fracture. In addition, discontinuation of denosumab may activate bone remodeling units in an area with microdamage accumulation in cortical bone caused by the previous bone suppression from the antiresorptive treatment. The activation of bone remodeling units may accelerate the occurrence of the atypical femoral fractures.     

Lipopolysaccharide-induced release of arachidonic acid and prostaglandins in liver macrophages: regulation by Group IV cytosolic phospholipase A2, but not by Group V and Group IIA secretory phospholipase A2.

Lipopolysaccharide (LPS) induces a delayed release (lag phase of 2-4 h) of arachidonic acid (AA) and prostaglandin (PG) D2 in rat liver macrophages. Group IV cytosolic phospholipase A2 (cPLA2) becomes phosphorylated within minutes after the addition of LPS. The phosphorylated form of cPLA2 shows an enhanced in vitro activity. The Ca2+ dependence of cPLA2 activity is not affected by phosphorylation of the enzyme. In addition, LPS induces an enhanced expression of cPLA2 mRNA (after 2-4 h) and an enhanced expression of cPLA2 protein (after 8 h). The cellular cPLA2 activity is enhanced about twofold 24 h after LPS treatment. Liver macrophages constitutively express mRNAs encoding Groups V and IIA secretory PLA2 (sPLA2). LPS has no effect on the levels of Groups V and IIA sPLA2 mRNA expression. Despite mRNA expression, Groups V and IIA sPLA2 protein and sPLA2 activity are not detectable in unstimulated or LPS-stimulated liver macrophages. Collectively, these and earlier [Mediators Inflammation 8 (1999) 295.] results suggest that in liver macrophages the LPS-induced delayed release of AA and prostanoids is mediated by phosphorylation and an enhanced expression of cPLA2, a de novo expression of cyclooxygenase (COX)-2, but not by the actions of Group V or Group IIA sPLA2.