Role of PII proteins in nitrogen fixation control of Herbaspirillum seropedicae strain SmR1

Background  

The PII protein family comprises homotrimeric proteins which act as transducers of the cellular nitrogen and carbon status in prokaryotes and plants. In Herbaspirillum seropedicae, two PII-like proteins (GlnB and GlnK), encoded by the genes glnB and glnK, were identified. The glnB gene is monocistronic and its expression is constitutive, while glnK is located in the nlmAglnKamtB operon and is expressed under nitrogen-limiting conditions.     

Education and data-intensive science in the beginning of the 21st century

Data-intensive science will open up new avenues to explore, new questions to ask, and new ways to answer. Yet, this potential cannot be unlocked without new emphasis on education of the researchers gathering data, the analysts analyzing data and the cross-disciplinary participants working together to make it happen. This article is a summary of the education issues and challenges of data-intensive sciences and cloud computing as discussed in the Data-Intensive Science (DIS) workshop in Seattle, September 19-20, 2010.     

The United States of America and Scientific Research

To gauge the current commitment to scientific research in the United States of America (US), we compared federal research funding (FRF) with the US gross domestic product (GDP) and industry research spending during the past six decades. In order to address the recent globalization of scientific research, we also focused on four key indicators of research activities: research and development (R&D) funding, total science and engineering doctoral degrees, patents, and scientific publications. We compared these indicators across three major population and economic regions: the US, the European Union (EU) and the People''s Republic of China (China) over the past decade. We discovered a number of interesting trends with direct relevance for science policy. The level of US FRF has varied between 0.2% and 0.6% of the GDP during the last six decades. Since the 1960s, the US FRF contribution has fallen from twice that of industrial research funding to roughly equal. Also, in the last two decades, the portion of the US government R&D spending devoted to research has increased. Although well below the US and the EU in overall funding, the current growth rate for R&D funding in China greatly exceeds that of both. Finally, the EU currently produces more science and engineering doctoral graduates and scientific publications than the US in absolute terms, but not per capita. This study''s aim is to facilitate a serious discussion of key questions by the research community and federal policy makers. In particular, our results raise two questions with respect to: a) the increasing globalization of science: “What role is the US playing now, and what role will it play in the future of international science?”; and b) the ability to produce beneficial innovations for society: “How will the US continue to foster its strengths?”     

Siderophore-controlled iron assimilation in the enterobacterium Erwinia chrysanthemi: evidence for the involvement of bacterioferritin and the Suf iron-sulfur cluster assembly machinery

The intracellular fate of iron acquired by bacteria during siderophore-mediated assimilation is poorly understood. We investigated this question in the pathogenic enterobacterium Erwinia chrysanthemi. This bacterium produces two siderophores, chrysobactin and achromobactin, during plant infection. We analyzed the distribution of iron into cytosolic proteins in bacterial cells supplied with 59Fe-chrysobactin using native gel electrophoresis. A parental strain and mutants deficient in bacterioferritin (bfr), miniferritin (dps), ferritin (ftnA), bacterioferredoxin (bfd), or iron-sulfur cluster assembly machinery (sufABCDSE) were studied. In the parental strain, we observed two rapidly 59Fe-labeled protein signals identified as bacterioferritin and an iron pool associated to the protein chain-elongation process. In the presence of increased 59Fe-chrysobactin concentrations, we detected mini-ferritin-bound iron. Iron incorporation into bacterioferritin was severely reduced in nonpolar sufA, sufB, sufD, sufS, and sufE mutants but not in a sufC background. Iron recycling from bacterioferritin did not occur in bfd and sufC mutants. Iron depletion caused a loss of aconitase activity, whereas ferric chrysobactin supplementation stimulated the production of active aconitase in parental cells and in bfr and bfd mutants. Aconitase activity in sufA, sufB, sufD, sufS, and sufE mutant strains was 10 times lower than that in parental cells. In the sufC mutant, it was twice as low as that in the parental strain. Defects observed in the mutants were not caused by altered ferric chrysobactin transport. Our data demonstrate a functional link between bacterioferritin, bacterioferredoxin, and the Suf protein machinery resulting in optimal bacterial growth and a balanced distribution of iron between essential metalloproteins.     

A logical analysis of the process of T cell activation: different consequences depending on the state of CD28 engagement

The adaptive immune system is a complex organized action of several immune cell types like, T cells, B cells, dendritic cells, mast cells, and their ability to recognize self and foreign molecular information. Based on logical analysis, a model has been developed that describes TCR-ligand association coupled to intracellular signaling events that result in a proliferation signal. The model demonstrates that after TCR-ligand binding, the activation of tyrosine kinases in one of the paths leads to oscillations between the subsequent states of activation and deactivation of Ca(2+) initiation. In our studies the effect of costimulation on the primary signal has also been explored. Analysis reveals that costimulation increases by more than 2.5 fold the number of paths rendering a cell proliferation signal compared to the outcome when costimulation is blocked. Traversal of 97% of these paths attains a costimulation threshold of activation. We also examined a hypothesis that couples the primary signal and costimulation by modeling costimulation to act as an inhibitor on the Inhibitor proteins. Using this hypothesis our analysis showed a 25% increase in the number of paths leading to cell proliferation in comparison to when costimulation is blocked. Our model also reveals that this hypothesis actually decrease by approximately 50% the number of paths attaining cell proliferation compared to the number of available paths leading to cell proliferation when costimulation does not act as an inhibitor on Inhibitor proteins. This suggests that costimulation influences cell proliferation by providing a greater diversity of paths that converge to this state. However, costimulation should be thought independent of its regulatory interaction with the inhibitor proteins.     

Patterns of cervical metastasis from carcinoma of the oral tongue

Background  

Cancer of the oral tongue is the second most common cancer among males in various parts of India. Despite advances in diagnosis and treatment the failure rates in cancer of the oral tongue are high and survival poor. Majority of these failures occur in untreated neck.     

Association of adenovirus early-region 1A proteins with cellular polypeptides.

Extracts from adenovirus-transformed human 293 cells were immunoprecipitated with monoclonal antibodies specific for the early-region 1A (E1A) proteins. In addition to the E1A polypeptides, these antibodies precipitated a series of proteins with relative molecular weights of 28,000, 40,000, 50,000, 60,000, 80,000, 90,000, 110,000, 130,000, and 300,000. The two most abundant of these polypeptides are the 110,000-molecular-weight protein (110K protein) and 300K protein. Three experimental approaches have suggested that the 110K and 300K polypeptides are precipitated because they form stable complexes with the E1A proteins. The 110K and 300K polypeptides do not share epitopes with the E1A proteins, they copurify with a subset of the E1A proteins, and they bind to the E1A proteins following mixing in vitro. The 110K and 300K polypeptides are not adenoviral proteins, but are encoded by cellular DNA. Both the 12S and the 13S E1A proteins bind to the 110K and 300K species, and these complexes are found in adenovirus-transformed and -infected cells.