Radboud University Nijmegen

Researchers have discovered a salt adaptation mechanism in plants that facilitates chloride removal from the roots and enhancing salinity tolerance. A research team has uncovered a novel mechanism of plant adaptation to salt stress involving the NaCl-induced translocation of a specific chloride channel protein, AtCLCf. National University of Singapore (NUS) researchers have discovered a salt adaptation mechanism in plants that facilitates chloride removal from the roots and enhancing salinity tolerance. Soil salinity is one of the most deleterious environmental stress factors and increased salinity poses a growing challenge for crop production and adversely affects crop yields worldwide. The excess accumulation of soluble salts, especially sodium chloride (NaCl), in the root zone severely impedes plant growth, reducing crop productivity. Although chloride ions (Cl-) are essential nutrients for plants at low concentrations, their excessive accumulation is toxic to the plant cells. Plants have evolved various strategies to cope with such environmental stresses by employing various channels and transporters for maintaining ion balance (ion homeostasis) in their cells. While there is a better understanding of the sodium ion homeostasis under salt stress, removal of chloride ions is not well understood. To address this, a research team led by Professor Prakash KUMAR from the NUS Department of Biological Sciences has uncovered a novel mechanism of plant adaptation to salt stress involving the NaCl-induced translocation of a specific chloride channel protein, AtCLCf. Their work revealed that the AtCLCf protein is made and stored in the endomembrane system (the Golgi apparatus) under normal growth conditions. When the root cells are treated with salt, AtCLCf translocates to the plasma membrane, where it helps to remove the excess chloride ions. This represents a novel mechanism to increase the plant's salinity tolerance. The research is a collaboration with Dr Ji?í FRIML from the Institute of Science and Technology, Austria and Professor XU Jian from Radboud University, The Netherlands. This work was recently published in Nature Communications on 10 May 2024. The study also identified a transcription factor, AtWRKY9, that directly regulates the expression of the AtCLCf gene when the plant is under salt stress. NaCl causes the AtCLCf protein to move from inside the cell (the Golgi) to the cell surface with the help of another protein called AtRABA1b/BEX5. If this movement is blocked by an inhibitor (brefeldin-A) or by modifying the BEX5 gene, it results in high salt sensitivity in plants. Transgenic plants designed to produce additional AtCLCf gene showed increased salt tolerance in mutant forms of Arabidopsis plants lacking the CLCf gene. Collectively, these findings proved that AtCLCf is involved in the removal of excess chloride ions from root tissues to increase the salt tolerance of plants. To understand how AtCLCf functions in plant cells, the researchers used several techniques such as fluorimetric measurement of liposomes incorporated with recombinant AtCLCf protein and chloride ion sensitive dye, as well as electrophysiological studies (patch clamp). These studies showed that AtCLCf works like a pump that swaps chloride ions with hydrogen ions, helping to remove excess chloride ions from the cells. Prof Kumar said, "This represents an essential and previously unknown salt tolerance mechanism in Arabidopsis plants. This knowledge could be used to improve the salinity tolerance of crop plants in the future."

While previous studies suggested an association of the most common cerebral small-vessel disease with dementia risk, new research provides evidence of causal link, identifying it as a major vascular factor. Research led by in part by The University of Texas Health Science Center at San Antonio (UT Health San Antonio) finds that the most common cerebral small-vessel disease feature seen in brain magnetic resonance imaging is a primary vascular factor associated with dementia risk. Results of the major international study emphasize the significance of that feature, known as white matter hyperintensity (WMH) burden, in preventive strategies for dementia. "Our findings provide converging evidence that WMH is a major vascular factor associated with dementia risk," said Muralidharan Sargurupremraj, PhD, an assistant professor at the Glenn Biggs Institute for Alzheimer's and Neurodegenerative Diseases at UT Health San Antonio. "They also support WMH as a surrogate marker for clinical trials to prevent dementia by controlling vascular risk." Sargurupremraj is the first and co-corresponding author of the research, titled, "Genetic Complexities of Cerebral Small Vessel Disease, Blood Pressure, and Dementia," published May 22 in JAMA Network Open, a monthly open-access medical journal published by the American Medical Association. The study notes that with increasing life expectancy, the prevalence of dementia is expected to reach 75 million people globally by 2030, which makes devising strategies to prevent or delay its occurrence a major public health priority. The scientific community widely recognizes that most dementia cases, including Alzheimer's disease, are related to a combination of vascular and neurodegenerative lesions. And cerebral small-vessel disease is thought to be the main underlying contribution to cognitive decline and dementia, with nearly half of dementia cases showing both Alzheimer's and cerebral small-vessel disease neuropathologic characteristics, the study notes. Still, while observational studies had shown evidence of an association between white matter hyperintensity burden and increased risk of stroke and dementia, causal evidence had been limited. White matter hyperintensities are lesions in the brain that show up as areas of increased brightness in T2-weighted magnetic resonance imaging. In the new study, researchers were able to provide evidence of a causal link between vascular traits and Alzheimer's disease, using genetic instrument variable analyses known as Mendelian randomization -- a method that leverages the natural randomization of genetic alleles to test how differences in the genetic effect on modifiable exposure influence disease risk. Specifically, in a two-year analysis ending July 24, 2022, and using Alzheimer's disease genome-wide association studies of up to 75,000 European dementia cases, they found causal evidence of an association of larger WMH burden with increased risk of the disease, accounting for pulse-pressure effects. The study also highlighted the importance of combining several complementary epidemiological approaches and data types, and of accounting for caveats of instrumental variable analyses when exploring the impact of vascular traits on late-onset diseases like dementia. "As vascular disease is a treatable contributor to dementia risk, our findings have broad significance for prevention strategies of Alzheimer's and dementia as a whole," Sargurupremraj concluded. The researchers advise future studies to examine whether their findings can be generalized to non-European populations. Other institutions and entities represented in the study include the University of Bordeaux (France); University of Washington; University of Michigan; University of Tartu (Estonia); Erasmus MC University Medical Center, Rotterdam (Netherlands); Boston University and the National Heart, Lung, and Blood Institute Framingham Heart Study; Icelandic Heart Association (Iceland); Washington University, St. Louis; University of Oxford (United Kingdom); Department of Public Health, Bordeaux (France); University of Pittsburgh; University of Lille (France); Radboud University, Nijmegen (Netherlands); Universidad Adolfo Ibáñez, Santiago (Chile); University of Iceland (Iceland); Oslo University Hospital, Oslo (Norway); Norwegian University of Science and Technology; Imperial College London (United Kingdom); National Institute on Aging; and Bordeaux University Hospital (France). UT Health San Antonio is a primary driver of San Antonio's leading $44.1 billion health care and biosciences sector, and is the largest academic research institution in South Texas with an annual research portfolio of $413 million.

timsTOF Ultra 2 enables significant further improvements in deep, high-fidelity 4D-Proteomics™ of mammalian cells, cancer cell lines, or tissue biopsies With sensitivity to measure >1000 proteins on just 25 pg, the timsTOF Ultra 2 opens new cell and disease biology research windows into PBMCs, small immune cells, bacterial cells, or subcellular organelle proteomics timsTOF Ultra 2 enables identification and quantitation of ~50% more protein groups and ~100% more peptides at 25 pg of digest sample with 1% FDR timsTOF Ultra 2 typically yields ~40% more peptides and ~20% more proteins for many other 4D-Proteomics applications with low-medium sample amounts Improved ion-charge control (ICC 2.0) method makes timsTOF Ultra 2 suitable for a very broad range of sample loading, from low picograms to micrograms New OmniScape™ top-down proteoform software for automated, near-complete protein sequence coverage from MALDI-ISD and LC-TIMS-MS/MS data Biognosys launches Spectronaut® 19 (SN19) with optimized AI for further increased depth of protein quantitation and greater peptide sequence coverage SN19 now specifically trained on timsTOF MS/MS for significant 4D-Proteomics performance improvements; SN19 now fully integrated into timsTOF Ultra 2 PreOmics launches reproducible and affordable deep plasma 4D-Proteomics ENRICHplus kit for 7-fold plasma depth improvement on robust timsTOF HT Novel capabilities for 4D-glycoprotein analysis: glyco-PASEF® and GlycoScape™ Bruker announces customer shipment of more than 1,000 timsTOF systems Bruker launches 3 mass spectrometers at ASMS 2024 for 4D-Proteomics, mass-spec multiomics tissue imaging, and for highest-confidence applied analysis ANAHEIM, Calif.--(BUSINESS WIRE)-- At the 72nd ASMS meeting, Bruker Corporation (Nasdaq: BRKR) launches the new top-of-the-line timsTOF Ultra 2 system with significantly further enhanced sensitivity for deep profiling of small cells, subcellular organelles, as well as increased sample loading flexibility. Together with new Spectronaut 19 software and the novel PreOmics ENRICHplus kit, Bruker is setting new 4D-Proteomics standards from highest sensitivity to large-scale, deep plasma proteomics. Bruker is also introducing OmniScape software for top-down sequence confirmation and de novo sequencing for intact, undigested proteoforms, dissociated in the mass spectrometer. This press release features multimedia. View the full release here: The new timsTOF Ultra 2 delivers ultimate sensitivity (Photo: Business Wire) Bruker Advances Ultimate Sensitivity with new timsTOF Ultra 2 The new timsTOF Ultra 2 delivers ultimate sensitivity of up to 50% more protein groups and up to 100% more peptides on just 25 pg of protein digest, i.e. only 1/10th the protein mass of a HeLa cell. This makes timsTOF Ultra 2 the best choice to investigate immune homeostasis surveying low abundance proteins from small peripheral blood mononuclear cells (PBMCs), or from bacterial cells comprising the microbiome, or for immunopeptidomics to discover cancer neoantigens from fine needle biopsies. New ion charge control (ICC2.0) software provides sample loading flexibility from low picogram amounts to about a microgram of protein digest. Bruker ProteoScape™ software now integrates Spectronaut 19 (SN19) software from Biognosys, the gold-standard for data-independent analysis (DIA). The new SN19 offers significantly improved search engine AI, advanced quantification, and allows precise predictions of timsTOF’s unique collision cross sections (DeepCCS), retention time (DeepiRT) and fragment ion intensity (DeepFrag), resulting in a 13% average increase in protein group identifications and improvements in quantification precision. See Biognosys Press Release Bruker once again intends to offer field upgrades to the timsTOF Ultra 2 for timsTOF Ultra/SCP customers. PreOmics launches Reproducible, Affordable ENRICHplus Deep Plasma 4D-Proteomics Solution, Leveraging the Proven Robustness of the timsTOF HT The new single particle PreOmics ENRICHplus kit and the timsTOF HT now deliver up to 7-fold improvement in protein identification and quantification versus neat plasma. The increased depth of coverage, together with field-proven throughput and robustness of the timsTOF HT enables deep plasma proteomics at scale. See PreOmics Press Release Dr. Roman Fischer, Associate Professor and Head of Discovery, Proteomics Facility, University of Oxford, UK, stated: "timsTOF technology, together with ENRICHplus, is changing the way we do plasma proteomics. On our timsTOF Pro we achieve on average 3800 protein identifications per sample with a throughput of 60 samples per day, while only using 20 µl of plasma. We never before achieved such depth with a single run of plasma, now enabling us to detect tissue leakage proteins and other low abundant potential biomarkers for cancer and neurodegenerative diseases. Together with the robust timsTOF system, ENRICHplus is game-changing for deep, affordable plasma proteomics at scale." Bruker Launches OmniScape Top-Down Software for Analysis of Intact Proteins Bruker is introducing OmniScape, the first top-down protein sequence software that covers protein de novo sequencing and lead sequence identification through homology searches for detailed proteoform analysis. Dr. Boris Krichel, University of Wisconsin-Madison, summarized: “I am excited about the de novo sequencing to discover and annotate proteins in untargeted top-down proteomics. The most impressive function of OmniScape is the automatic suggestion of matching proteoforms based on multiple variable modifications.” OmniScape supports different data types from LC-CCS-MS/MS, enabling for example the analysis of multiply phosphorylated proteins. Its ability to integrate different datasets yields very high sequence coverages, providing reliable sequence calls and PTMs. OmniScape can also process MALDI-ISD top-down spectra from the timsTOF fleX and axial MALDI instruments including the new neofleX, as well as data from non-Bruker instruments as a one-for-all top-down protein sequencing and isoform determination software solution. Dr. Christian Isak Jørgensen, Senior Science Manager, Novonesis, Denmark, added: “OmniScape addresses a real need in the biotech industry producing recombinant proteins.” Novel Acquisition and Computational Capabilities for 4D-Glycoproteomics Bruker is introducing GlycoScape, the first real-time glycoproteomic software. GlycoScape has been developed in collaboration with the Radboud University Medical Center in the public-private partnership project EnFORCE led by Dr. Hans Wessels [1]. The software can identify glycopeptides on-the-fly as data are acquired and without the need to rely on glycan libraries, not only enabling identification of previously unreported glycans, but significantly minimizing false negative results. The unbiased read-out of glycoproteomic data by GlycoScape is critical for the advancement of glycobiology in translational and clinical research as these important research fields become accessible in the post-genomic era. Dr. Hans Wessels, Senior Researcher at Radboud University in Nijmegen highlighted key advantages: “GlycoScape opens up the analysis of glycoproteomic mass spectrometry data from the timsTOF platform for on-the-fly processing without glycan database restrictions.” GlycoScape leverages the glyco-PASEF method for ultra-sensitive and rapid glycoprotein data acquisition, using stepped energy CID and oxonium-ion-gated polygon-filtering, that was developed in collaboration with Prof. Albert Heck’s group at Utrecht University. Dr. Albert Heck, Professor of Chemistry and Pharmaceutical Sciences at Utrecht University and Scientific Director of the Netherlands Proteomics Center, noted: “I am pleased with our pioneering work in leveraging the unique strengths of the timsTOF platform for glycoproteomics, now translated to the glyco-PASEF method for research in glycobiology.” [1] The collaboration project is co-funded by PPP Allowance awarded by Health~Holland, Top Sector Life Sciences & Health, to stimulate public-private partnerships (Grant #LSHM21032). About Bruker Corporation – the Emerging Leader of the Post-Genomic Era Bruker is enabling scientists and engineers to make breakthrough post-genomic discoveries and develop new applications that improve the quality of human life. Bruker’s high-performance scientific instruments and high-value analytical and diagnostic solutions enable scientists to explore life and materials at molecular, cellular, and microscopic levels. In close cooperation with our customers, Bruker is enabling innovation, improved productivity, and customer success in post-genomic life science molecular and cell biology research, in applied and biopharma applications, in microscopy and nanoanalysis, as well as in industrial and cleantech research, and next-gen semiconductor metrology in support of AI. Bruker offers differentiated, high-value life science and diagnostics systems and solutions in preclinical imaging, clinical phenomics research, proteomics and multiomics, spatial and single-cell biology, functional structural and condensate biology, as well as in clinical microbiology and molecular diagnostics. For more information, please visit .