bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nectar bacteria stimulate pollen germination and bursting to enhance their fitness
Authors: Christensen S. M. , Munkres I. , Vannette R. L. 
Published: January 2021

AbstractFor many flower visitors, pollen is the primary source of non-carbon nutrition, but pollen has physical defenses that make it difficult for consumers to access nutrients. Nectar-dwelling microbes are nearly ubiquitous among flowers and can reach high densities, despite the fact that floral nectar is nitrogen limited, containing only very low concentrations of non-carbon nutrients. Pollen contains trace micronutrients and high protein content but is protected by a recalcitrant outer shell. Here, we report that a common genus of nectar-dwelling bacteria,Acinetobacter, exploits pollen nutrition by inducing pollen germination and bursting. We use time course germination assays to quantify the effect ofAcinetobacterspecies on pollen germination and pollen bursting. Inoculation withAcinetobacterspecies resulted in increased germination rates within 15 minutes, and bursting by 45 minutes, as compared to uninoculated pollen. The pollen germination and bursting phenotype is density-dependent, with lower concentrations of A.pollinisSCC477 resulting in a longer lag time before the spike in germination, which is then closely followed by a spike in bursting. Lastly,A. pollinisgrows to nearly twice the density with germinable pollen vs ungerminable pollen, indicating that their ability to induce and exploit germination plays an important role in rapid growth. To our knowledge, this is the first direct test of non-plant biological induction of pollen germination, as well as the first evidence of induced germination as a method of nutrient procurement, as the microbes appear to hijack the pollen’s normally tightly controlled germination mechanisms for their benefit. Our results suggest that further study of microbe-pollen interactions may inform many aspects of pollination ecology, including microbial ecology in flowers, the mechanisms of pollinator nutrient acquisition from pollen, and cues of pollen germination for plant reproduction.
Is Palmer’s elm leaf goldenrod real? The Angiosperms353 kit provides within-species signal inSolidago ulmifolias.l
Authors: Beck James B. , Markley Morgan L. , Zielke Mackenzie G. , Thomas Justin R. , Hale Haley J. , Williams Lindsay D. , Johnson Matthew G. 
Published: January 2021

AbstractThe genusSolidagorepresents a taxonomically challenging group due to its sheer number of species, putative hybridization, polyploidy, and shallow genetic divergence among species. Here we use a dataset obtained exclusively from herbarium specimens to evaluate the status ofSolidago ulmifoliavar.palmeri,a morphologically subtle taxon potentially confined to Alabama, Arkansas, Mississippi, and Missouri. A multivariate analysis of both discrete and continuous morphological data revealed no clear distinction betweenS. ulmifoliavar.palmeriandSolidago ulmifoliavar.ulmifolia. Solidago ulmifoliavar.palmeri’s status was also assessed with a phylogenomic and SNP clustering analysis of data generated with the “Angiosperms353” probe kit. Neither analysis supportedSolidago ulmifoliavar.palmerias a distinct taxon, and we suggest that this name should be discarded. The status ofSolidago delicatula(formerly known asSolidago ulmifoliavar.microphylla)was also assessed. Both morphological and phylogenic analyses supported the species status ofS. delicatulaand we suggest maintaining this species at its current rank. These results highlight the utility of the Angiosperms353 probe kit, both with herbarium tissue and at lower taxonomic levels. Indeed, this is the first study to utilize this kit to identify genetic groups within a species.
Synthetic Promoter Designs Enabled by a Comprehensive Analysis of Plant Core Promoters
Authors: Jores Tobias , Tonnies Jackson , Wrightsman Travis , Buckler Edward S. , Cuperus Josh T. , Fields Stanley , Queitsch Christine 
Published: January 2021

AbstractTargeted engineering of plant gene expression holds great promise for ensuring food security and for producing biopharmaceuticals in plants. However, this engineering requires thorough knowledge ofcis-regulatory elements in order to precisely control either endogenous or introduced genes. To generate this knowledge, we used a massively parallel reporter assay to measure the activity of nearly complete sets of promoters from Arabidopsis, maize and sorghum. We demonstrate that core promoter elements – notably the TATA-box – as well as promoter GC content and promoter-proximal transcription factor binding sites influence promoter strength. By performing the experiments in two assay systems, leaves of the dicot tobacco and protoplasts of the monocot maize, we detect species-specific differences in the contributions of GC content and transcription factors to promoter strength. Using these observations, we built computational models to predict promoter strength in both assay systems, allowing us to design highly active promoters comparable in activity to the viral 35S minimal promoter. Our results establish a promising experimental approach to optimize native promoter elements and generate synthetic ones with desirable features.
A role for prefoldins in H2A.Z deposition inArabidopsis
Authors: Marí-Carmona Cristina , Forment Javier , Blázquez Miguel A. , Alabadí David 
Published: January 2021

ABSTRACTThe prefoldin complex (PFDc) participates in cellular proteostasis in eukaryotes by acting as cochaperone of the chaperonin CTT. This role is mainly exerted in the cytoplasm where it contributes to the correct folding of client proteins, thus preventing them to form aggregations and cellular damage. Several reports indicate, however, that they also play a role in transcriptional regulation in the nucleus in several model species. In this work, we have investigated how extended is the role of PFDs in nuclear processes by inspecting their interactome and their coexpression networks in yeast, fly, and humans. The analysis indicates that they may perform extensive, conserved functions in nuclear processes. The construction of the predicted interactome forArabidopsisPFDs, based on the ortholog interactions, has allowed us to identify many putative PFD interactors linking them to unanticipated processes, such as chromatin remodeling. Based on this analysis, we have investigated the role of PFDs in H2A.Z deposition through their interaction with the chromatin remodeling complex SWR1c. Our results show that PFDs have a positive effect on SWR1c, which is reflected in defects in H2A.Z deposition in hundreds of genes in seedlings defective in PFD3 and PFD5 activities.
Identification of hub molecules of FUS-ALS by Bayesian gene regulatory network analysis of iPSC model: iBRN
Authors: Nogami Masahiro , Ishikawa Mitsuru , Doi Atsushi , Sano Osamu , Sone Takefumi , Akiyama Tetsuya , Aoki Masashi , Nakanishi Atsushi , Ogi Kazuhiro , Yano Masato , Okano Hideyuki 
Published: January 2021

SUMMARYFused in sarcoma/translated in liposarcoma (FUS) is a causative gene of amyotrophic lateral sclerosis (ALS). Mutated FUS causes accumulation of DNA damage and cytosolic stress granule (SG) formation, thereby motor neuron (MN) death. However, key molecular aetiology remains unclear. Here, we applied a novel platform technology, iBRN, “Non-biased”Bayesian gene regulatorynetwork analysis based oninduced pluripotent stem cell (iPSC)-derived cell model, to elucidate the molecular aetiology using transcriptome of iPSC-derived MNs harboring FUSH517D. iBRN revealed “hub molecules”, which strongly influenced transcriptome network, such as miR-125b-5p-TIMELESS axis and PRKDC for the molecular aetiology. Next, we confirmed miR-125b-5p-TIMELESS axis in FUSH517DMNs such that miR-125b-5p regulated several DNA repair-related genes including TIMELESS. In addition, we validated both introduction of miR-125b-5p and knocking down of TIMELESS caused DNA damage in the cell culture model. Furthermore, PRKDC was strongly associated with FUS mis-localization into SGs by DNA damage under impaired DNA-PK activity. Collectively, our iBRN strategy provides the first compelling evidence to elucidate molecular aetiology in neurodegenerative diseases.HighlightsA new platform technology, “iBRN”, Bayesian gene regulatory network analysis based on iPSC cellsiBRN identifies hub molecules to strongly influence the gene network in FUS-ALSPRKDC specifically acts as a guardian against FUS mis-localization during DNA damage stressmiR-125b-5p-TIMELESS axis regulates DNA repair-related genes in FUS-ALS.
Leishmania donovanimetacyclic promastigotes impair phagosome properties in inflammatory monocytes
Authors: Matte Christine , Duque Guillermo Arango , Descoteaux Albert 
Published: January 2021

AbstractLeishmaniasis, a debilitating disease with clinical manifestations ranging from self-healing ulcers to life-threatening visceral pathologies, is caused by protozoan parasites of theLeishmaniagenus. These professional vacuolar pathogens are transmitted by infected sand flies to mammalian hosts as metacyclic promastigotes and are rapidly internalized by various phagocyte populations. Classical monocytes are among the first myeloid cells to migrate to infection sites. Recent evidence shows that recruitment of these cells contributes to parasite burden and to the establishment of chronic disease. However, the nature ofLeishmania-inflammatory monocyte interactions during the early stages of host infection has not been well investigated. Here, we aimed to assess the impact ofLeishmania donovanimetacyclic promastigotes on antimicrobial responses within these cells. Our data showed that inflammatory monocytes were readily colonized byL. donovanimetacyclic promastigotes, while infection withEscherichia coliwas efficiently cleared. Upon internalization, metacyclic promastigotes inhibited superoxide production at the parasitophorous vacuole (PV) through a mechanism involving exclusion of NADPH oxidase subunits gp91phoxand p47phoxfrom the PV membrane. Moreover, we observed that unlike phagosomes enclosing zymosan particles, vacuoles containing parasites acidified poorly. Interestingly, whereas the parasite surface coat virulence glycolipid lipophosphoglycan was responsible for the inhibition of PV acidification, impairement of the NADPH oxidase assembly was independent of lipophosphoglycan and of the metalloprotease GP63. Collectively, these observations indicate that permissiveness of inflammatory monocytes toL. donovanimay thus be related to the ability of this parasite to impair the microbicidal properties of phagosomes.
Association of Inflammation with Depression and Anxiety: Evidence for Symptom-Specificity and Potential Causality from UK Biobank and NESDA Cohorts
Authors: Milaneschi Yuri , Kappelmann Nils , Ye Zheng , Lamers Femke , Moser Sylvain , Jones Peter B. , Burgess Stephen , Penninx Brenda W. J. H. , Khandaker Golam M. 
Published: January 2021

ABSTRACTWe examined whether inflammation is uniformly associated with all depressive and anxiety symptoms, and whether these associations are potentially causal. Data was from 147,478 individuals from the UK Biobank (UKB) and 2,905 from the Netherlands Study of Depression and Anxiety (NESDA). Circulating C-reactive protein (CRP) was measured in both cohorts and interleukin-6 (IL-6) in NESDA. Genetic instruments for these proteins were obtained from published GWAS and UKB. Depressive and anxiety symptoms were assessed with self-report questionnaires. In NESDA, neurovegetative (appetite, sleep, psychomotor) symptoms were disaggregated as increased vs. decreased. In joint analyses, circulating CRP was associated with depressive symptoms of depressed mood (OR=1.06, 95%CI=1.05-1.08), altered appetite (OR=1.25, 95%CI=1.23-1.28), sleep problems (OR=1.05, 95%CI=1.04-1.06), and fatigue (OR=1.12, 95%CI=1.11-1.14), and with anxiety symptoms of irritability (OR=1.06, 95%CI=1.05-1.08) and worrying control (OR=1.03, 95%CI=1.02-1.04). Further analyses in NESDA using IL-6 as exposure confirmed associations with depressive symptoms, including anhedonia (OR=1.30, 95%CI=1.12-1.52). Both CRP (OR=1.27, 95%CI=1.13-1.43) and IL-6 (OR=1.26, 95%CI=1.07-1.49) were associated with increased sleep. CRP was associated with increased appetite (OR=1.21, 95%CI=1.08-1.35) while IL-6 with decreased appetite (OR=1.45, 95%CI=1.18-1.79). In Mendelian Randomization analyses, increased risk of fatigue (estimate=0.25, SE=0.08) and sleep problems (estimate=0.19, SE=0.07) were associated with genetically-predicted higher IL-6 activity. Inflammation was associated with core depressive symptoms of low mood and anhedonia and somatic/neurovegetative symptoms of fatigue, altered sleep and appetite changes. Less consistent associations were found for anxiety. The IL-6/IL-6R pathway could be causally linked to depression. Experimental studies are required to further evaluate causality, mechanisms, and usefulness of immunotherapies for depressive symptoms.
Polygenic Risk Scores for Alzheimer’s Disease and Mild Cognitive Impairment in Hispanics/Latinos in the U.S: The Study of Latinos – Investigation of Neurocognitive Aging
Authors: Sofer Tamar , Kurniansyah Nuzulul , Granot-Hershkovitz Einat , Goodman Matthew O. , Tarraf Wassim , Broce Iris , Lipton Richard B. , Daviglus Martha , Lamar Melissa , Wassertheil-Smoller Sylvia , Cai Jianwen , DeCarli Charles S. , Gonzalez Hector M. , Fornage Myriam 
Published: January 2021

AbstractIntroductionPolygenic Risk Score (PRS) are powerful summaries of genetic risk alleles that can potentially be used to predict disease outcomes and guide treatment decisions. Hispanics/Latinos suffer from higher rates of Alzheimer’s Disease (AD) and Mild Cognitive Impairment (MCI) compared to non-Hispanic Whites, yet the strongest known genetic risk factor for AD, APOE-ϵ4 allele, has weak association with AD in Hispanics/Latinos. We evaluated PRS constructed based on Genome-Wide Association Studies (GWAS) of AD in predicting MCI in Hispanics/Latinos when accounting for APOE alleles and variants.MethodsWe used summary statistics from four GWAS of AD to construct PRS that predict MCI in 4,189 diverse Hispanics/Latinos (mean age 63 years, 47% males) from the Study of Latinos-Investigation of Neurocognitive Aging. We assessed the PRS associations with MCI in the combined set of people and in groups defined by genetic ancestry and Hispanic/Latino background, and when including and excluding single nucleotide polymorphisms (SNPs) from the APOE gene region.ResultsA PRS constructed based on GWAS of AD in the FINNGEN Biobank was associated with MCI (OR = 1.34, 95% CI [1.15, 1.55]), and its association was mostly driven by 158 APOE region SNPs. A PRS constructed based on a multi-ethnic AD GWAS was associated with MCI (OR=1.22, 95% CI [1.08, 1.37]) without including any APOE region SNPs. APOE-ϵ4 and APOE-ϵ2 alleles were not associated with MCI.DiscussionA combination of APOE region SNPs is associated with MCI in Hispanics/Latinos despite APOE-ϵ4 and APOE-ϵ2 alleles not being associated with MCI.
Weighted burden analysis in 200,000 exome-sequenced subjects characterises rare variant effects on risk of type 2 diabetes
Authors: Curtis David 
Published: January 2021

AbstractType 2 diabetes (T2D) is a disease for which both common genetic variants and environmental factors influence risk. A few genes have been identified in which very rare variants have large effects on risk and here we carry out a weighted burden analysis of rare variants in a sample of over 200,000 exome-sequenced participants in the UK Biobank project, of whom over 13,000 have T2D. Variant weights were allocated based on allele frequency and predicted effect, as informed by a previous analysis of hyperlipidaemia. There was an exome-wide significant increased burden of rare, functional variants in three genes,GCK, HNF4AandGIGYF1. GIGYF1has not previously been identified as a diabetes risk gene but its product is plausibly involved in the modification of insulin signalling. A number of other genes did not attain exome-wide significance but were highly ranked and potentially of interest, includingALAD, PPARG, GYG1andGHRL. Loss of function (LOF) variants were associated with T2D inGCKandGIGYF1whereas nonsynonymous variants annotated as probably damaging were associated inGCKandHNF4A. Overall, fewer than 1% of T2D cases carried one of these variants. In two genes previously implicated in diabetes aetiology,HNF1AandHNF1B, there was an excess of LOF variants among cases but the small numbers of these fell well short of statistical significance, suggesting that even larger datasets will be helpful for more fully elucidating the contribution of rare genetic variants to T2D risk. This research has been conducted using the UK Biobank Resource.
Migration and Outbreaks of Vaccine-Preventable Disease in Europe: A Systematic Review
Authors: Deal Anna , Halliday Rachael , Crawshaw Alison , Hayward Sally , Burnard Amelia , Rustage Kieran , Carter Jessica , Mehrotra Anushka , Knights Felicity , Campos-Matos Ines , Majeed Azeem , Friedland Jon S. , Edelstein Michael , Mounier-Jack Sandra , Hargreaves Sally ,   in collaboration with the ESCMID Study Group for Infections in Travellers and Migrants (ESGITM)
Published: January 2021

AbstractBackgroundMigrant populations (defined as foreign-born) are one of several under-immunised groups in the EU/EEA, yet little is known about how they are affected by outbreaks of vaccine-preventable diseases (VPDs). This information is vital to develop targeted strategies to improve the health of diverse migrant communities and to assess risk factors and correlations with major European peaks in incidence of key VPDs over time.MethodsWe did a systematic review (PROSPERO CRD42019157473; Medline, EMBASE, and Global Health January 2000 to October 2019) adhering to PRISMA guidelines, to identify studies on VPD outbreaks (measles, mumps, rubella, diphtheria, pertussis, polio, hepatitis A,N meningitidis, andH influenzae) in migrants residing in the EU/EEA and Switzerland.Results45 studies were included, reporting on 47 distinct VPD outbreaks across 13 countries (26 [55%] were reported between 2010 and 2020, including 16 [34%] since 2015). Most reported outbreaks involving migrants were of measles (n=24; 6578 total cases), followed by varicella (n=11; 596 cases), hepatitis A (n=7; 1510 cases), rubella (n=3; 487 cases) and mumps (n=2; 295 cases). 19 (40%) of outbreaks, predominantly varicella and measles, were reported in temporary camps or shelters for asylum seekers and refugees. Of 11 varicella outbreaks, 82% were associated with adult migrants. Half of measles outbreaks (n=12) were associated with migrants from Eastern European countries, often involving migrants of Roma ethnicity.ConclusionsMigrants represent one of several under-immunised groups involved in VPD outbreaks in Europe, with adult and child refugees and asylum seekers residing in shelters or temporary camps at particular risk, alongside specific nationality groups. Vulnerability varies by disease, setting, and individual demographics, highlighting the importance of tailoring strategies for implementing catch-up vaccination to specific groups, alongside the strengthening of routine data collection, in order to meet regional and global vaccination targets. Better understanding vaccine uptake and demand issues in migrant groups, and reducing the barriers they face to accessing vaccination services, is urgently needed, with direct implications for COVID-19 vaccine delivery at the current time. Strengthening vaccine delivery to migrant populations will require a greater focus on co-designing vaccine uptake strategies in close collaboration with affected communities.FunderNIHR
Heart rate variability predicts decline in sensorimotor rhythm control
Authors: Nann Marius , Haslacher David , Colucci Annalisa , Eskofier Bjoern , von Tscharner Vinzenz , Soekadar Surjo R. 
Published: January 2021

AbstractVoluntary control of sensorimotor rhythms (SMR, 8-12 Hz) can be used for brain-computer interface (BCI)-based operation of an assistive hand exoskeleton, e.g., in finger paralysis after stroke. To gain SMR control, stroke survivors are usually instructed to engage in motor imagery (MI) or to attempt moving the paralyzed fingers resulting in task- or event-related desynchronization (ERD) of SMR (SMR-ERD). However, as these tasks are cognitively demanding, especially for stroke survivors suffering from cognitive impairments, BCI control performance can deteriorate considerably over time. It would thus be important to identify biomarkers that predict decline in BCI control performance within an ongoing session in order to optimize the man-machine interaction scheme. Here we determine the link between BCI control performance over time and heart rate variability (HRV). Specifically, we investigated whether HRV can be used as a biomarker to predict decline during voluntary control of SMR-ERD across 17 healthy participants using Granger causality. SMR-ERD was visually displayed on a screen. Participants were instructed to engage in MI-based SMR-ERD control over two consecutive runs of 8.5 minutes each. During the second run, task difficulty was gradually increased. While control performance (p= .18) and HRV (p= .16) remained unchanged across participants during the first run, during the second run, both measures declined over time at high correlation (performance: -0.61%/10s,p= 0; HRV: -0.007ms/10s,p< .001). We found that HRV Granger-caused BCI control performance (p< .001) exhibited predictive characteristics of HRV on an individual participant level. These results suggest that HRV can predict decline in BCI performance paving the way for adaptive BCI control paradigms, e.g., to individualize and optimize assistive BCI systems in stroke.
Competitive binding of STATs to receptor phospho-Tyr motifs accounts for altered cytokine responses in autoimmune disorders
Authors: Wilmes Stephan , Jeffrey Polly-Anne , Martinez-Fabregas Jonathan , Hafer Maximillian , Fyfe Paul , Pohler Elizabeth , Gaggero Silvia , López-García Martín , Lythe Grant , Guerrier Thomas , Launay David , Suman Mitra , Piehler Jacob , Molina-París Carmen , Moraga Ignacio 
Published: January 2021

ABSTRACTCytokines elicit pleiotropic and non-redundant activities despite strong overlap in their usage of receptors, JAKs and STATs molecules. We use IL-6 and IL-27 to ask how two cytokines activating the same signaling pathway have different biological roles. We found that IL-27 induces more sustained STAT1 phosphorylation than IL-6, with the two cytokines inducing comparable levels of STAT3 phosphorylation. Mathematical and statistical modelling of IL-6 and IL-27 signaling identified STAT3 binding to GP130, and STAT1 binding to IL-27Rα, as the main dynamical processes contributing to sustained pSTAT1 by IL-27. Mutation of Tyr613 on IL-27Rα decreased IL-27-induced STAT1 phosphorylation by 80% but had limited effect on STAT3 phosphorylation. Strong receptor/STAT coupling by IL-27 initiated a unique gene expression program, which required sustained STAT1 phosphorylation and IRF1 expression and was enriched in classical Interferon Stimulated Genes. Interestingly, the STAT/receptor coupling exhibited by IL-6/IL-27 was altered in patients with Systemic lupus erythematosus (SLE). IL-6/IL-27 induced a more potent STAT1 activation in SLE patients than in healthy controls, which correlated with higher STAT1 expression in these patients. Partial inhibition of JAK activation by sub-saturating doses of Tofacitinib specifically lowered the levels of STAT1 activation by IL-6. Our data show that receptor and STATs concentrations critically contribute to shape cytokine responses and generate functional pleiotropy in health and disease.