bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Chlamydomonas Genome Project, version 6: reference assemblies for mating type plus and minus strains reveal extensive structural mutation in the laboratory
Authors: Craig Rory J. , Gallaher Sean D. , Shu Shengqiang , Salomé Patrice , Jenkins Jerry W. , Blaby-Haas Crysten E. , Purvine Samuel O. , O’Donnell Samuel , Barry Kerrie , Grimwood Jane , Strenkert Daniela , Kropat Janette , Daum Chris , Yoshinaga Yuko , Goodstein David M. , Vallon Olivier , Schmutz Jeremy , Merchant Sabeeha S. 
Published: June 2022

ABSTRACTFive versions of the Chlamydomonas reinhardtii reference genome have been produced over the last two decades. Here we present version 6, bringing significant advances in assembly quality and structural annotations. PacBio-based chromosome-level assemblies for two laboratory strains, CC-503 and CC-4532, provide resources for the plus and minus mating type alleles. We corrected major misassemblies in previous versions and validated our assemblies via linkage analyses. Contiguity increased over ten-fold and >80% of filled gaps are within genes. We used Iso-Seq and deep RNA-seq datasets to improve structural annotations, and updated gene symbols and textual annotation of functionally characterized genes via extensive curation. We discovered that the cell wall-less classical reference strain CC-503 exhibits genomic instability potentially caused by deletion of RECQ3 helicase, with major structural mutations identified that affect >100 genes. We therefore present the CC-4532 assembly as the primary reference, although this strain also carries unique structural mutations and is experiencing rapid proliferation of a Gypsy retrotransposon. We expect all laboratory strains to harbor gene-disrupting mutations, which should be considered when interpreting and comparing experimental results across laboratories and over time. Collectively, the resources presented here herald a new era of Chlamydomonas genomics and will provide the foundation for continued research in this important reference.
Drug-induced change in transmitter identity is a shared mechanism generating cognitive deficits
Authors: Marta Pratelli , Hakimi Anna M. , Thaker Arth , Li Hui-quan , Godavarthi Swetha K. , Spitzer Nicholas C. 
Published: June 2022

AbstractCognitive deficits are a long-lasting consequence of drug use, yet the convergent mechanism by which classes of drugs with different pharmacological properties cause similar deficits is unclear. We find that both phencyclidine and methamphetamine, despite differing in their targets in the brain, impair memory by causing the same glutamatergic neurons in the medial prefrontal cortex to gain a GABAergic phenotype and decrease their expression of the vesicular glutamate transporter. Suppressing drug-induced gain of GABA with RNA-interference prevents the appearance of memory deficits. Drug-induced prefrontal hyperactivity drives this change in transmitter identity. Normalizing the activity of prefrontal glutamatergic neurons after drug-exposure reverses the gain of GABAergic phenotype and rescues the associated memory deficits. Increased activity of dopaminergic neurons in the ventral tegmental area is necessary and sufficient to produce the change in transmitter identity. The results reveal a shared and reversible mechanism by which exposure to different drugs causes cognitive deficits.
Nascent dendrite branches initiated by a localized burst of Spire-dependent actin polymerization
Authors: Hatton Deirdre , Marquilly Claire , Hanrahan Caitlin , Ferreira Tiago , Ou Yimiao , Cinq-Mars Lauren , Silkworth Will , Bailey Hannah M. , Quinlan Margot E. , van Meyel Donald J. 
Published: June 2022

SummaryDendrites form arbors whose size, shape and complexity define how neurons cover their receptive territories. Actin dynamics contribute to growth and remodeling of dendrite arbors. Here we examined how Spire, a conserved actin nucleation factor, promotes formation of new branches in vivo. In live imaging of Drosophila class IV dendritic arborization (c4da) neurons, Spire was observed at new sites of branch initiation, where it assembled new actin polymer in a burst just prior to filopodial outgrowth. For dendrite arborization, Spire required intact structural domains to nucleate actin and target the secretory network, and interacted with Rab11 GTPase, a key regulator of recycling endosomes. Together, these findings support a model in which Spire cooperates with Rab11 to promote new dendrite branches by linking localized actin dynamics with intracellular trafficking of endosomes that deliver lipids and cargoes to fuel protrusive outgrowth of nascent dendrites.
Use of a citizen science tool for the determination of biological invasions in urban areas
Authors: Botan Ana Luiza Moreira , Heringer Gustavo , de Matos Ana Carolina Lacerda , Oliveira Daniel Luiz , Ramos de Alvarenga Danielle , Wilson Almeida Jonathan , Palmieri Tavares Karla , Lopes Bueno Marina , Lopes Vitor Hugo , Zenni Rafael Dudeque 
Published: June 2022

AbstractUrban environments are critical points for biological invasions because these areas are susceptible to a greater number of environmental disturbances. Because they are densely populated ecosystems, urban environments present a unique opportunity for the involvement of society in the management of invasive exotic species. Similarly, citizen science offers opportunities to conduct research in the field of ecology together with society. The objective of our study was to analyze the occurrence of exotic species in urban areas recorded on iNaturalist and determine whether citizen science applications are good data sources for research projects in invasion ecology. Specifically, we evaluated whether richness and composition of the exotic species community in the cities registered on the iNaturalist platform were explained by socioeconomic and environmental factors. We also verified whether richness of the exotic species in cities registered on the iNaturalist platform were similar to the richness of the exotic species community in the region where the city is located using data collected only by researchers. We obtained 38,374 occurrences of 265 invasive species covering 2,057 cities in 72 countries. Occurrence records were concentrated in North America, Western Europe and Oceania, and there were no data for cities in most of Africa, the Middle East, Eastern Europe and West Asia. Socioeconomic and environmental factors were important determinants of the richness of exotic species in urban areas of the world and were important determinants of the richness of exotic species in natural environments. Urban hotspots of invasive exotic species were different from those for ecosystems in general.
Fish environmental DNA in lake sediment overcomes the gap of reconstructing past fauna in lake ecosystems
Authors: Sakata Masayuki K. , Tsugeki Narumi , Kuwae Michinobu , Ochi Natsuki , Hayami Kana , Osawa Ryohei , Morimoto Teppei , Yasashimoto Tetsu , Takeshita Daiki , Doi Hideyuki , Minamoto Toshifumi 
Published: June 2022

AbstractUnderwater sediments are a natural archive of biological information. Reconstruction of past fauna has been conducted for various taxonomic groups using morphological remains and DNA derived from these remains. However, information on past occurrences of fish species, the top predator of lake ecosystems, could have been reproduced only in exceptional environments, and past quantitative information on fish, particularly in lake ecosystems, has been a knowledge gap in reconstructing past fauna. Tracking the quantitative fluctuations of fish is essential for reconstructing multiple trophic levels of organisms in lake ecosystems.To acquire past quantitative fish information from lake sediments, we collected approximately 30 cm-length of underwater sediments in Lake Biwa. We extracted sedimentary environmental DNA (eDNA) and measured temporal fluctuations in the eDNA concentration of the native and fishery target speciesPlecoglossus altivelisandGymnogobius isaza. ForP. altivelis, we examined the possibility of tracking quantitative fluctuations by comparing sedimentary eDNA with recorded catch per unit effort (CPUE).The chronology of the sediments allowed us to obtain information on sediments collected in Lake Biwa over the past 100 years. The deepest depths at which sedimentary eDNA was detected were 30 and 13 cm forP. altivelisandG. isazafrom the surface, corresponding to approximately 100 and 30 years ago, respectively. In the comparison of sedimentary eDNA concentrations and biomass, we found a significant correlation between the CPUE ofP. altivelisand its sedimentary eDNA concentration adjusted to compensate for DNA degradation. Sedimentary eDNA fluctuations were observed inP. altivelis, possibly reflecting the abundance fluctuation due to variations in the main food resources of zooplankton.Our findings provide essential pieces for the reconstruction of past fauna of lake ecosystems. The addition of quantitative information on fish species will reach a new phase, for instance, by investigating population shifts or biological interactions in the reconstruction of past fauna in lake ecosystems.
Epsin2, a novel target for multiple system atrophy therapy via α-synuclein/FABP7 propagation
Authors: Cheng An , Kawahata Ichiro , Wang Yifei , Jia Wenbin , Sekimori Tomoki , Chen Yi , Stefanova Nadia , Finkelstein David I , Ma Wenbo , Chen Min , Sasaki Takuya , Fukunaga Kohji 
Published: June 2022

SUMMARYMultiple system atrophy (MSA) is a neurodegenerative disease showing accumulation of misfolded α-synuclein and myelin disruption. However, the mechanism how α-synuclein (α-syn) accumulate in MSA brain remains unclear. Here, we identify the protein epsin-2 as a novel target for MSA therapy via controlling α-synuclein accumulation. In MSA mouse model, PLP-hαSyn transgenic mice and FABP7/α-syn hetero-aggregates injected mice, we firstly found that fatty acid-binding protein 7 (FABP7) related to MSA development and formed hetero-aggregates with α-syn, which exhibited stronger toxicity than α-syn aggregates. Furthermore, injected FABP7/α-syn hetero-aggregates in mice selectively accumulated in oligodendrocytes and Purkinje neurons and cause cerebellar dysfunction. By bioinformatic analyses, the protein epsin-2 expresses in both oligodendrocyte and Purkinje cells was found as a potential target to regulate FABP7/α-syn hetero-aggregates propagation via clathrin-dependent endocytosis. The AAV5-dependent epsin-2 knock-down mice exhibited decreased levels of aggregates accumulation in Purkinje neurons and oligodendrocytes as well as performed improved myelin levels and Purkinje neurons in cerebellum and motor functions. Thus, we propose epsin-2 as a novel and therapeutic candidate for MSA.
Translation, reliability, and validity of Amharic versions of the Pelvic Floor Distress Inventory (PFDI-20) and Pelvic Floor Impact Questionnaire (PFIQ-7)
Authors: Melkie Tadesse Belayneh , Gashaw Zelalem Mengistu , Workineh Zelalem Ayichew , Andargie Tamiru Minwuye , Debele Tibeb Zena , Nigatu Solomon Gedlu 
Published: June 2022

AbstractPurposePelvic Floor Disorders (PFDs) affects many women and have a significant impact on their quality of life. Pelvic Floor Impact Questionnaire (PFIQ-7) and Pelvic Floor Distress Inventory (PFDI-20) help to assess PFDs; however, both are not culturally translated into the Amharic-language. Hence, we aimed to translate the English versions of short forms of the PFDI-20 and PFIQ-7 into Amharic-language and evaluate their psychometric properties in Amharic-speaking Ethiopian women with symptomatic PFDs.MethodsThe PFDI-20 and PFIQ-7 were translated into Amharic language using standard procedures. The Amharic versions were completed by 197 patients (response rate 92%) with PFDs from University of Gondar specialized and comprehensive Hospital. Internal consistency and test-retest reliability were examined through Cronbach’s alpha and Intraclass correlation coefficients (ICC). A relative criterion standard, POP-SS-7 score, was correlated with total PFDI-20 and subscale POPDI-6 scores (spearman’s rank order correlation (SCC). Construct validity was evaluated by known group validity using the Mann–Whitney U test.ResultsBoth instruments were successfully translated and adapted with an excellent content validity (> 0.90). The Amharic versions of the PFDI-20 and PFIQ-7 showed excellent internal consistency and test-retest reliability in both summary and subscales (Cronbach’s alpha: 0.92 for PFDI-20 and 0.91 for PFIQ-7; and ICC: 0.97 for PFDI-20 and 0.86 for PFIQ-7). Criterion validity was good for POPDI-6 (SCC = 0.71; p < 0.001). Moreover, construct validity was acceptable, showing significant differences among groups of PFDs in the PFDI-20 and PFIQ-7 scores (Mann–Whitney U Test; p < 0.001).ConclusionsThe Amharic versions of the PFDI-20 and PFIQ-7 are comprehensible, reliable, valid, and feasible in Ethiopian Amharic-speaking women with PFDs to evaluate symptoms and its impact during research and clinical practice. However, further studies are needed to evaluate the responsiveness.
Nasal DNA methylation at three CpG sites predicts childhood allergic disease
Authors: van Breugel Merlijn , Qi Cancan , Xu Zhongli , Pedersen Casper-Emil Tingskov , Petoukhov Ilya , Vonk Judith M. , Gehring Ulrike , Berg Marijn , Bügel Marnix , Capraij Orestes A. , Forno Erick , Morin Andréanne , Eliasen Anders Ulrik , Jiang Yale , van den Berge Maarten , Nawijn Martijn C. , Li Yang , Chen Wei , Bont Louis , Bønnelykke Klaus , Celedón Juan C. , Koppelman Gerard H. , Xu Cheng-Jian 
Published: June 2022

AbstractChildhood allergic diseases, including asthma, rhinitis and eczema, are prevalent conditions that share strong genetic and environmental components. Diagnosis relies on clinical history and measurements of allergen-specific IgE. We hypothesized that a multi-omics model could accurately diagnose childhood allergic disease. We show that nasal DNA methylation has by far the strongest predictive power to diagnose childhood allergy, surpassing blood DNA methylation, genetic risk scores, and environmental factors. DNA methylation at only three nasal CpG sites classifies allergic disease in Dutch children, with an area under the curve (AUC) of 0.86. This was replicated in US Hispanic children (AUC 0.82). DNA methylation at these CpGs additionally detects allergic multimorbidity and symptomatic IgE sensitization. Using nasal single-cell RNA-sequencing data, we map these three CpG sites to reflect the influx of T cells and macrophages that contribute to allergic inflammation. Our study offers a simple, non-invasive diagnostic test for childhood allergy.
A machine learning model to aid detection of familial hypercholesterolaemia
Authors: Gratton Jasmine , Futema Marta , Humphries Steve E. , Hingorani Aroon D. , Finan Chris , Schmidt A. Floriaan 
Published: June 2022

2.TEXT ABSTRACT AND KEYWORDSBackground and AimsPeople with monogenic familial hypercholesterolaemia (FH) are at an increased risk of premature coronary heart disease and death. Currently there is no population screening strategy for FH, and most carriers are identified late in life, delaying timely and cost-effective interventions. The aim was to derive an algorithm to improve detection of people with monogenic FH.MethodsA penalised (LASSO) logistic regression model was used to identify predictors that most accurately identified people with a higher probability of FH in 139,779 unrelated participants of the UK Biobank, including 488 FH carriers. Candidate predictors included information on medical and family history, anthropometric measures, blood biomarkers, and an LDL-C polygenic score (PGS). Model derivation and evaluation was performed using a random split of 80% training and 20% testing data.ResultsA 14-variable algorithm for FH was derived, where the top five variables included triglyceride, LDL-C, and apolipoprotein A1 concentrations, self-reported statin use, and an LDL-C PGS. Model evaluation in the test data resulted in an area under the curve (AUC) of 0.77 (95% CI: 0.71; 0.83), and appropriate calibration (calibration-in-the-large: -0.07 (95% CI: -0.28; 0.13); calibration slope: 1.02 (95% CI: 0.85; 1.19)). Employing this model to prioritise people with suspected monogenic FH is anticipated to reduce the number of people requiring sequencing by 88% compared to a population-wide sequencing screen, and by 18% compared to prioritisation based on LDL-C and statin use.ConclusionsThe detection of individuals with monogenic FH can be improved with the inclusion of additional non-genetic variables and a PGS for LDL-C.
A G protein coupled receptor like protein systematically modulates nutrient-growth by Ca2+mediated phosphatidylcholine perception during evolutionary adaptation
Authors: Huang Zhixiong , He Xue , Zhao Xueqiang , Teng Wan , Hu Mengyun , Zhang Yijing , Li Junming , Li Hui , Tong Yiping 
Published: June 2022

AbstractNutrients are important for growth in both plants and animals, uncovering of signaling pathway in nutrients determined growth is essential. Here we clonedTaPCGR1-3B(Phospholipid Coordinated Growth and nutrients Response1), controlled by SNPs on alternative splicing and transcription factors binding, conferring nitrogen deficiency response. TaPCGR1-3B was localized in plasma membrane and endoplasmic reticulum of meristem cell. Nitrogen deprivation stimulated interaction of TaPCGR1-3B with G protein alpha subunit and phospholipase C 9, which was inhibited by phosphatidylcholine, to trigger Ca2+signaling and inhibit normal growth. Knockdown ofTaPCGR1rescued the growth inhibition caused by nutrient deficient conditions by modulation of phosphatidylcholine induced growth gene expression through Ca2+signaling disruption. Modulating of phosphatidylcholine mediatedTaPCGR1activity thus tightly regulated growth through Ca2+signaling.
Single-cell atlas of bronchoalveolar lavage from preschool cystic fibrosis reveals new cell phenotypes
Authors: Maksimovic Jovana , Shanthikumar Shivanthan , Howitt George , Hickey Peter F , Ho William , Anttila Casey , Brown Daniel V. , Senabouth Anne , Kaczorowski Dominik , Amann-Zalcenstein Daniela , Powell Joseph E. , Ranganathan Sarath C. , Oshlack Alicia , Neeland Melanie R. 
Published: June 2022

ABSTRACTInflammation is a key driver of cystic fibrosis (CF) lung disease, not addressed by current standard care. Improved understanding of the mechanisms leading to aberrant inflammation may assist the development of effective anti-inflammatory therapy. Single-cell RNA sequencing (scRNA-seq) allows profiling of cell composition and function at previously unprecedented resolution. Herein, we seek to use multimodal single-cell analysis to comprehensively define immune cell phenotypes, proportions and functional characteristics in preschool children with CF. We analyzed 42,658 cells from bronchoalveolar lavage of 11 preschool children with CF and a healthy control using scRNA-seq and parallel assessment of 154 cell surface proteins. Validation of cell types identified by scRNA-seq was achieved by assessment of samples by spectral flow cytometry. Analysis of transcriptome expression and cell surface protein expression, combined with functional pathway analysis, revealed 41 immune and epithelial cell populations in BAL. Spectral flow cytometry analysis of over 256,000 cells from a subset of the same patients revealed high correlation in major cell type proportions across the two technologies. Macrophages consisted of 13 functionally distinct sub populations, including previously undescribed populations enriched for markers of vesicle production and regulatory/repair functions. Other novel cell populations included CD4 T cells expressing inflammatory IFNα/β and NFκB signalling genes. Our work provides a comprehensive cellular analysis of the pediatric lower airway in preschool children with CF, reveals novel cell types and provides a reference for investigation of inflammation in early life CF.
Landscape drives zoonotic malaria prevalence in non-human primates
Authors: Johnson Emilia , Kumar Sharma Reuben Sunil , Cuenca Pablo Ruiz , Byrne Isabel , Salgado-Lynn Milena , Shahar Zarith Suraya , Lin Lee Col , Zulkifli Norhadila , Mohd Saidi Nor Dilaila , Drakeley Chris , Matthiopoulos Jason , Nelli Luca , Fornace Kimberly 
Published: June 2022

ABSTRACTZoonotic disease dynamics in wildlife hosts are rarely quantified at macroecological scales due to the lack of systematic surveys. Non-human primates (NHPs) hostPlasmodium knowlesi,a zoonotic malaria of public health concern and the main barrier to malaria elimination in Southeast Asia. Understanding of regionalP. knowlesiinfection dynamics in wildlife is limited. Here, we systematically assemble reports of NHPP. knowlesiand investigate geographic determinants of prevalence in reservoir species. Meta-analysis of 6322 NHPs from 148 sites reveals that prevalence is heterogeneous across Southeast Asia, with low overall prevalence and high estimates for Malaysian Borneo. We find that regions exhibiting higher prevalence in NHPs overlap with human infection hotspots. In wildlife and humans, parasite transmission is linked to land conversion and fragmentation. By assembling remote sensing data and fitting statistical models to prevalence at multiple spatial scales, we identify novel relationships betweenP. knowlesiin NHPs and forest fragmentation. This suggests that higher prevalence may be contingent on habitat complexity, which would begin to explain observed geographic variation in parasite burden. These findings address critical gaps in understanding regionalP. knowlesiepidemiology and indicate that prevalence in simian reservoirs may be a key spatial driver of human spillover risk.
Nuclear fascin regulates cancer cell survival
Authors: Lawson Campbell D. , Peel Samantha , Jayo Asier , Corrigan Adam , Iyer Preeti , Dalrymple Mabel Baxter , Marsh Richard J. , Cox Susan , Van Audenhove Isabel , Gettemans Jan , Parsons Maddy 
Published: June 2022

AbstractFascin is an important regulator of F-actin bundling leading to enhanced filopodia assembly. Fascin is also overexpressed in most solid tumours where it supports invasion through control of F-actin structures at the periphery and nuclear envelope. Recently fascin has been identified in the nucleus of a broad range of cell types but the contributions of nuclear fascin to cancer cell behaviour remain unknown. Here we demonstrate that fascin bundles F-actin within the nucleus to support chromatin organisation and efficient DNA damage response. Fascin associates directly with phosphorylated Histone H3 leading to regulated levels of nuclear fascin to support these phenotypes. Forcing nuclear fascin accumulation through the expression of nuclear-targeted fascin-specific nanobodies or inhibition of Histone H3 kinases results in enhanced and sustained nuclear F-actin bundling leading to reduced invasion, viability and nuclear fascin-specific/driven apoptosis. These findings represent an additional important route through which fascin can support tumorigenesis and provide insight into potential pathways for targeted fascin-dependent cancer cell killing.