34 research outputs found
A Public–Industry Partnership for Enhancing Corn Nitrogen Research and Datasets: Project Description, Methodology, and Outcomes
Due to economic and environmental consequences of N lost from fertilizer applications in corn (Zea mays L.), considerable public and industry attention has been devoted to the development of N decision tools. Needed are research and databases and associated metadata, at numerous locations and years to represent a wide geographic range of soil and weather scenarios, for evaluating tool performance. The goals of this research were to conduct standardized corn N rate response field studies to evaluate the performance of multiple public-domain N decision tools across diverse soils and environmental conditions, develop and publish new agronomic science for improved crop N management, and train new scientists. The geographic scope, scale, and unique collaborative arrangement warrant documenting details of this research. The objectives of this paper are to describe how the research was undertaken, reasons for the methods, and the project’s anticipated value. The project was initiated in a partnership between eight U.S. Midwest land-grant universities, USDA-ARS, and DuPont Pioneer. Research using a standardized protocol was conducted over the 2014 through 2016 growing seasons, yielding a total of 49 sites. Preliminary observations of soil and crop variables measured from each site revealed a magnitude of differences in soil properties (e.g., texture and organic matter) as well as differences in agronomic and economic responses to applied N. The project has generated a valuable dataset across a wide array of weather and soils that allows investigators to perform robust evaluation of N use in corn and N decision tools
Occlusion of Regulatory Sequences by Promoter Nucleosomes In Vivo
Nucleosomes are believed to inhibit DNA binding by transcription factors. Theoretical attempts to understand the significance of nucleosomes in gene expression and regulation are based upon this assumption. However, nucleosomal inhibition of transcription factor binding to DNA is not complete. Rather, access to nucleosomal DNA depends on a number of factors, including the stereochemistry of transcription factor-DNA interaction, the in vivo kinetics of thermal fluctuations in nucleosome structure, and the intracellular concentration of the transcription factor. In vitro binding studies must therefore be complemented with in vivo measurements. The inducible PHO5 promoter of yeast has played a prominent role in this discussion. It bears two binding sites for the transcriptional activator Pho4, which at the repressed promoter are positioned within a nucleosome and in the linker region between two nucleosomes, respectively. Earlier studies suggested that the nucleosomal binding site is inaccessible to Pho4 binding in the absence of chromatin remodeling. However, this notion has been challenged by several recent reports. We therefore have reanalyzed transcription factor binding to the PHO5 promoter in vivo, using ‘chromatin endogenous cleavage’ (ChEC). Our results unambiguously demonstrate that nucleosomes effectively interfere with the binding of Pho4 and other critical transcription factors to regulatory sequences of the PHO5 promoter. Our data furthermore suggest that Pho4 recruits the TATA box binding protein to the PHO5 promoter
The NANOGrav 15-year Data Set: Observations and Timing of 68 Millisecond Pulsars
We present observations and timing analyses of 68 millisecond pulsars (MSPs)
comprising the 15-year data set of the North American Nanohertz Observatory for
Gravitational Waves (NANOGrav). NANOGrav is a pulsar timing array (PTA)
experiment that is sensitive to low-frequency gravitational waves. This is
NANOGrav's fifth public data release, including both "narrowband" and
"wideband" time-of-arrival (TOA) measurements and corresponding pulsar timing
models. We have added 21 MSPs and extended our timing baselines by three years,
now spanning nearly 16 years for some of our sources. The data were collected
using the Arecibo Observatory, the Green Bank Telescope, and the Very Large
Array between frequencies of 327 MHz and 3 GHz, with most sources observed
approximately monthly. A number of notable methodological and procedural
changes were made compared to our previous data sets. These improve the overall
quality of the TOA data set and are part of the transition to new pulsar timing
and PTA analysis software packages. For the first time, our data products are
accompanied by a full suite of software to reproduce data reduction, analysis,
and results. Our timing models include a variety of newly detected astrometric
and binary pulsar parameters, including several significant improvements to
pulsar mass constraints. We find that the time series of 23 pulsars contain
detectable levels of red noise, 10 of which are new measurements. In this data
set, we find evidence for a stochastic gravitational-wave background.Comment: 90 pages, 74 figures, 6 tables; published in Astrophysical Journal
Letters as part of Focus on NANOGrav's 15-year Data Set and the Gravitational
Wave Background. For questions or comments, please email
[email protected]
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Dysregulation of Exosome Cargo by Mutant Tau Expressed in Human-induced Pluripotent Stem Cell (iPSC) Neurons Revealed by Proteomics Analyses.
Accumulation and propagation of hyperphosphorylated Tau (p-Tau) is a common neuropathological hallmark associated with neurodegeneration of Alzheimer's disease (AD), frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), and related tauopathies. Extracellular vesicles, specifically exosomes, have recently been demonstrated to participate in mediating Tau propagation in brain. Exosomes produced by human induced pluripotent stem cell (iPSC)-derived neurons expressing mutant Tau (mTau), containing the P301L and V337M Tau mutations of FTDP-17, possess the ability to propagate p-Tau pathology after injection into mouse brain. To gain an understanding of the mTau exosome cargo involved in Tau pathogenesis, these pathogenic exosomes were analyzed by proteomics and bioinformatics. The data showed that mTau expression dysregulates the exosome proteome to result in 1) proteins uniquely present only in mTau, and not control exosomes, 2) the absence of proteins in mTau exosomes, uniquely present in control exosomes, and 3) shared proteins which were significantly upregulated or downregulated in mTau compared with control exosomes. Notably, mTau exosomes (not control exosomes) contain ANP32A (also known as I1PP2A), an endogenous inhibitor of the PP2A phosphatase which regulates the phosphorylation state of p-Tau. Several of the mTau exosome-specific proteins have been shown to participate in AD mechanisms involving lysosomes, inflammation, secretases, and related processes. Furthermore, the mTau exosomes lacked a substantial portion of proteins present in control exosomes involved in pathways of localization, vesicle transport, and protein binding functions. The shared proteins present in both mTau and control exosomes represented exosome functions of vesicle-mediated transport, exocytosis, and secretion processes. These data illustrate mTau as a dynamic regulator of the biogenesis of exosomes to result in acquisition, deletion, and up- or downregulation of protein cargo to result in pathogenic mTau exosomes capable of in vivo propagation of p-Tau neuropathology in mouse brain
Recommended from our members
Dysregulation of Exosome Cargo by Mutant Tau Expressed in Human-induced Pluripotent Stem Cell (iPSC) Neurons Revealed by Proteomics Analyses.
Accumulation and propagation of hyperphosphorylated Tau (p-Tau) is a common neuropathological hallmark associated with neurodegeneration of Alzheimer's disease (AD), frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), and related tauopathies. Extracellular vesicles, specifically exosomes, have recently been demonstrated to participate in mediating Tau propagation in brain. Exosomes produced by human induced pluripotent stem cell (iPSC)-derived neurons expressing mutant Tau (mTau), containing the P301L and V337M Tau mutations of FTDP-17, possess the ability to propagate p-Tau pathology after injection into mouse brain. To gain an understanding of the mTau exosome cargo involved in Tau pathogenesis, these pathogenic exosomes were analyzed by proteomics and bioinformatics. The data showed that mTau expression dysregulates the exosome proteome to result in 1) proteins uniquely present only in mTau, and not control exosomes, 2) the absence of proteins in mTau exosomes, uniquely present in control exosomes, and 3) shared proteins which were significantly upregulated or downregulated in mTau compared with control exosomes. Notably, mTau exosomes (not control exosomes) contain ANP32A (also known as I1PP2A), an endogenous inhibitor of the PP2A phosphatase which regulates the phosphorylation state of p-Tau. Several of the mTau exosome-specific proteins have been shown to participate in AD mechanisms involving lysosomes, inflammation, secretases, and related processes. Furthermore, the mTau exosomes lacked a substantial portion of proteins present in control exosomes involved in pathways of localization, vesicle transport, and protein binding functions. The shared proteins present in both mTau and control exosomes represented exosome functions of vesicle-mediated transport, exocytosis, and secretion processes. These data illustrate mTau as a dynamic regulator of the biogenesis of exosomes to result in acquisition, deletion, and up- or downregulation of protein cargo to result in pathogenic mTau exosomes capable of in vivo propagation of p-Tau neuropathology in mouse brain