bluuebunny/crossref_metadata_2025_split huggingface dataset:
Increased microclimatic variation in artificial nests does not create ecological traps for a secondary cavity breeder
Authors: Schwartz Timothée , Genouville Arnaud , Besnard Aurélien 
Published: May 2020

AbstractArtificial devices are increasingly used in conservation measures to mitigate the disappearance of natural habitats. However, few studies have demonstrated their benefits for the target species, and they may pose a risk of creating ecological traps. This occurs when lower individual fitness is found in artificial habitats that are more attractive than their natural equivalents. In this study, we tested the ecological trap hypothesis on a dense population of European rollersCoracias garrulusbreeding in both natural cavities and nest-boxes. Our initial hypothesis was that the more stressful microclimatic conditions of nest-boxes would lead to reduced fitness of rollers, thus creating an ecological trap. The results showed that nest-boxes were preferred over natural cavities. Despite significantly more extreme microclimatic conditions in nest-boxes, we found similar breeding parameters between artificial and natural nest types. Our results also suggest that rollers selected the nest-boxes which best buffered the temperature, thus avoiding potential ecological traps. Overall our results lead to the conclusion that nest-boxes do not create ecological traps for rollers in this study site. However, other species may be more sensitive to microclimatic variations or less able to avoid the least favourable nest-boxes. These findings could help to inform the placement of nest-boxes in order to reduce extreme temperatures and variation in humidity rates. Future studies could compare nest types for other fitness parameters, such as juvenile body condition or survival. We also recommend the ecological trap hypothesis as a useful framework to evaluate the outcomes of artificial devices used for conservation.
A freshwater radiation of diplonemids
Authors: Mukherjee Indranil , Salcher Michaela M , Andrei Adrian-Ştefan , Kavagutti Vinicius Silva , Shabarova Tanja , Grujčić Vesna , Haber Markus , Layoun Paul , Hodoki Yoshikuni , Nakano Shin-ichi , Šimek Karel , Ghai Rohit 
Published: May 2020

AbstractDiplonemids are considered marine protists and have been reported among the most abundant and diverse eukaryotes in the world oceans. Recently we detected the presence of freshwater diplonemids in Lake Biwa, Japan. However, their distribution and abundances in freshwater ecosystems remain unknown. We assessed abundance and diversity of diplonemids from several geographically distant deep freshwater lakes of the world by amplicon-sequencing, shotgun metagenomics and CARD-FISH. We found diplonemids in all the studied lakes, albeit with low abundances and diversity. We assembled long 18S rRNA sequences from freshwater diplonemids and showed that they form a new lineage distinct from the diverse marine clades. Freshwater diplonemids are a sister-group to marine isolates from coastal and bay areas, suggesting a recent habitat transition from marine to freshwater habitats. Images of CARD-FISH targeted freshwater diplonemids suggest they feed on bacteria. Our analyses of 18S rRNA sequences retrieved from single cell genomes of marine diplonemids shows they encode multiple rRNA copies that may be very divergent from each other, suggesting that marine diplonemid abundance and diversity both have been overestimated. These results have wider implications on assessing eukaryotic abundances in natural habitats by using amplicon-sequencing alone.
Non-canonical autophagy drives alternative ATG8 conjugation to phosphatidylserine
Authors: Durgan Joanne , Lystad Alf H. , Sloan Katherine , Carlsson Sven R. , Wilson Michael I. , Marcassa Elena , Ulferts Rachel , Webster Judith , Lopez-Clavijo Andrea F. , Wakelam Michael J. , Beale Rupert , Simonsen Anne , Oxley David , Florey Oliver 
Published: May 2020

AbstractAutophagy is a fundamental catabolic process essential for development, homeostasis and proper immune function1. During autophagy, a cascade of ATG proteins target intracellular cargoes for lysosomal degradation and recycling2. This pathway utilises a unique post-translational modification, the conjugation of ATG8 proteins to phosphatidylethanolamine (PE) at autophagosomes, which modulates cargo selection and maturation. ATG8 lipidation also occurs during non-canonical autophagy, a parallel pathway involving Single Membrane ATG8 Conjugation (SMAC) to endolysosomal compartments, which plays a key role in phagocytosis and other processes3. It has been widely assumed that SMAC involves the same lipidation of ATG8 to PE, but this has yet to be formally tested. Here, we show that ATG8 undergoes alternative lipidation to phosphatidylserine (PS) during non-canonical autophagy/SMAC. Using mass spectrometry, we find that activation of SMAC, by pharmacological agents4,5, or during non-canonical autophagy processes such as LC3-associated phagocytosis6,7and Influenza A virus infection8, induces the covalent conjugation of ATG8 to PS, as well as PE. This alternative lipidation event is dependent on the ATG16L1 WD40 domain, and occurs at PS enriched endolysosomal membranes. Importantly, we find that the ATG8-PS and ATG8-PE adducts are differentially delipidated by isoforms of the ATG4 family, indicating significant molecular distinctions and mechanisms between these two species.Together, these results provide an important new insight into autophagy signalling, revealing an alternative form of the hallmark ATG8-lipidation event, so widely used to define and assay autophagy. Furthermore, ATG8-PS lipidation provides a specific ‘molecular signature’ for non-canonical autophagy, uncovering a novel means of detecting and monitoring this emerging pathway.
Evidence that polyploidy in esophageal adenocarcinoma originates from mitotic slippage caused by defective chromosome attachments
Authors: Scott Stacey J. , Li Xiaodun , Jammula Sriganesh , Devonshire Ginny , Lindon Catherine , Fitzgerald Rebecca C. , D’Avino Pier Paolo 
Published: May 2020

AbstractPolyploidy is present in many cancer types and is increasingly recognized as an important factor in promoting chromosomal instability, genome evolution, and heterogeneity in cancer cells. However, the mechanisms that trigger polyploidy in cancer cells are largely unknown. In this study, we investigated the origin of polyploidy in esophageal adenocarcinoma (EAC), a highly heterogenous cancer, using a combination of genomics and cell biology approaches in EAC cell lines, organoids, and tumors. We found the EAC cells and organoids present specific mitotic defects consistent with problems in the attachment of chromosomes to the microtubules of the mitotic spindle. Time-lapse analyses confirmed that EAC cells have problems in congressing and aligning their chromosomes, which can ultimately culminate in mitotic slippage and polyploidy. Furthermore, whole-genome sequencing, RNA-seq, and quantitative immunofluorescence analyses revealed alterations in the copy number, expression, and cellular distribution of several proteins known to be involved in the mechanics and regulation of chromosome dynamics during mitosis. Together, these results provide evidence that an imbalance in the amount of proteins implicated in the attachment of chromosomes to spindle microtubules is the molecular mechanism underlying mitotic slippage in EAC. Our findings that the likely origin of polyploidy in EAC is mitotic failure caused by problems in chromosomal attachments not only improves our understanding of cancer evolution and diversification, but may also aid in the classification and treatment of EAC and possibly other highly heterogeneous cancers.
Stress-induced translation inhibition through rapid displacement of scanning initiation factors
Authors: Bresson Stefan , Shchepachev Vadim , Spanos Christos , Turowski Tomasz , Rappsilber Juri , Tollervey David 
Published: May 2020

SUMMARYCellular responses to environmental stress are frequently mediated by RNA-binding proteins (RBPs). Here, we examined global RBP dynamics inSaccharomyces cerevisiaein response to glucose starvation and heat shock. Each stress induced rapid remodeling of the RNA-protein interactome, without corresponding changes in RBP abundance. Consistent with general translation shutdown, ribosomal proteins contacting the mRNA showed decreased RNA-association. Among translation components, RNA-association was most reduced for initiation factors involved in 40S scanning (eIF4A, eIF4B, and Ded1), indicating a common mechanism of translational repression. In unstressed cells, eIF4A, eIF4B, and Ded1 primarily targeted the 5′-ends of mRNAs. Following glucose withdrawal, 5’-binding was abolished within 30sec, explaining the rapid translation shutdown, but mRNAs remained stable. Heat shock induced progressive loss of 5’ RNA-binding by initiation factors over ∼16min. Translation shutoff provoked selective 5′-degradation of mRNAs encoding translation-related factors, mediated by Xrn1. These results reveal mechanisms underlying translational control of gene expression during stress.HighlightsA quantitative proteomic approach reveals rapid stress-induced changes in RNA-binding Translation shutdown is driven by loss of mRNA binding by scanning initiation factors eIF4B and Ded1 have key but separate roles in driving the stress response Heat shock invokes rapid RNA degradation by Xrn1, selective for translation machinery
LiBis: An ultrasensitive alignment method for low-input bisulfite sequencing
Authors: Yin Yue , Li Jia , Li Jin , Lee Minjung , Zhao Sibo , Guo Linlang , Li Jianfang , Zhang Mutian , Huang Yun , Li Xiao-Nan , Sun Deqiang 
Published: May 2020

AbstractThe cell-free DNA (cfDNA) methylation profile in liquid biopsies has been utilized to diagnose early-stage disease and estimate therapy response. However, in typical clinical settings, only very small amounts of cfDNA can be purified. Whole-genome bisulfite sequencing (WGBS) is the gold standard to measure DNA methylation; however, WGBS using small amounts of fragmented DNA introduces a critical challenge for data analysis, namely a low mapping ratio. This, in turn, generates low sequencing depth and low coverage for CpG sites genome wide. The lack of informative CpGs has become a bottleneck for the clinical application of cfDNA-based WGBS assays. Hence, we developed LiBis (Low-input Bisulfite Sequencing), a novel method for low-input WGBS data alignment. By dynamically clipping initially unmapped reads and remapping clipped fragments, we judiciously rescued those reads and uniquely aligned them to the genome. By substantially increasing the mapping ratio by up to 88%, LiBis dramatically improved the number of informative CpGs and the precision in quantifying the methylation status of individual CpG sites. The high sensitivity and cost effectiveness afforded by LiBis for low-input samples will allow the discovery of genetic and epigenetic features suitable for downstream analysis and biomarker identification using liquid biopsy.
Expression changes in immune and epigenetic gene pathways associated with nutritional metabolites in maternal blood from pregnancies resulting in autism and atypical neurodevelopment
Authors: Zhu Yihui , Mordaunt Charles E. , Durbin-Johnson Blythe P , Caudill Marie A , Malysheva Olga V. , Miller Joshua W. , Green Ralph , James S. Jill , Melnyk Stepan B. , Fallin M. Daniele , Hertz-Picciotto Irva , Schmidt Rebecca J. , LaSalle Janine M. 
Published: May 2020

AbstractBackgroundThe prenatal period is a critical window to study factors involved in the development of autism spectrum disorder (ASD). Environmental factors, especiallyin uteronutrition, can interact with genetic risk for ASD, but how specific prenatal nutrients in mothers of children later diagnosed with ASD or non-typical development (Non-TD) associate with gestational gene expression is poorly understood. Maternal blood collected prospectively during pregnancy provides a new opportunity to gain insights into nutrition, particularly one-carbon metabolites, on gene pathways and neurodevelopment.MethodsGenome-wide transcriptomes were measured using microarrays in 300 maternal blood samples from all three trimesters in the Markers of Autism Risk in Babies - Learning Early Signs (MARBLES) study. Sixteen different one-carbon metabolites, including folic acid, betaine, 5’-methyltretrahydrofolate (5-MeTHF), and dimethylglycine (DMG) were measured. Differential expression analysis and weighted gene correlation network analysis (WGCNA) were used to compare gene expression between children later diagnosed as typical development (TD), Non-TD and ASD, and to nutrient metabolites.ResultsUsing differential gene expression analysis, six transcripts associated with four genes (TGR-AS1, SQSTM1, HLA-CandRFESD) showed genome-wide significance (FDRq< 0.05) with child outcomes. Genes nominally differentially expressed compared to TD specifically in ASD, but not Non-TD, significantly overlapped with seven high confidence ASD genes. 218 transcripts in common to ASD and Non-TD differential expression compared to TD were significantly enriched for functions in immune response to interferon-gamma, apoptosis, and metal ion transport. WGCNA identified co-expressed gene modules significantly correlated with 5-MeTHF, folic acid, DMG, and betaine. A module enriched in DNA methylation functions showed a protective association with folic acid/5-MeTHF concentrations and ASD risk. Independent of child outcome, maternal plasma betaine and DMG concentrations associated with a block of co-expressed genes enriched for adaptive immune, histone modification, and RNA processing functions.LimitationsBlood contains a heterogeneous mixture of cell types, and many WGCNA modules correlated with cell type and/or nutrient concentrations, but not child outcome. Gestational age correlated with some co-expressed gene modules in addition to nutrients.ConclusionsThese results support the premise that the prenatal maternal blood transcriptome is a sensitive indicator of gestational nutrition and children’s later neurodevelopmental outcomes.
p53 induces ARTS to promote mitochondrial apoptosis
Authors: Hao Qian , Chen Jiaxiang , Liao Junming , Huang Yingdan , Larisch Sarit , Zeng Shelya X , Lu Hua , Zhou Xiang 
Published: May 2020

AbstractApoptosisRelated protein inTGF-βSignaling pathway (ARTS) was originally discovered in cells undergoing apoptosis in response to TGF-β, but ARTS also acts downstream of many other apoptotic stimuli. ARTS induces apoptosis by antagonizing the anti-apoptotic proteins XIAP and Bcl-2. Here, we identified the pro-apoptoticSept4/ARTSgene as a p53-responsive target gene. Ectopic p53 and a variety of p53-inducing agents increased both mRNA and protein levels of ARTS, whereas ablation of p53 reduced ARTS expression in response to multiple stress conditions. Also, γ-irradiation induced p53-dependent ARTS expression in mice. Consistently, p53 binds to the responsive DNA element on the ARTS promoter and transcriptionally activated the promoter-driven expression of a luciferase reporter gene. Interestingly, ARTS binds to and sequesters p53 at mitochondria, enhancing the interaction of the latter with Bcl-XL. Ectopic ARTS markedly augments DNA damage stress- or Nutlin-3-triggered apoptosis, while ablation of ARTS preferentially impairs p53-induced apoptosis. Altogether, these findings demonstrate that ARTS collaborates with p53 in mitochondria-engaged apoptosis.
Expression of ACE2 and TMPRSS2 proteins in the upper and lower aerodigestive tracts of rats
Authors: Sato Taku , Ueha Rumi , Goto Takao , Yamauchi Akihito , Kondo Kenji , Yamasoba Tatsuya 
Published: May 2020

AbstractObjectivePatients with coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), exhibit not only respiratory symptoms but also symptoms of chemo-sensitive disorders and kidney failure. Cellular entry of SARS-CoV-2 depends on the binding of its spike protein to a cellular receptor named angiotensin-converting enzyme 2 (ACE2), and the subsequent spike protein-priming by host cell proteases, including transmembrane protease serine 2 (TMPRSS2). Thus, high expression of ACE2 and TMPRSS2 are considered to enhance the invading capacity of SARS-CoV-2.MethodsTo elucidate the underlying histological mechanisms of the aerodigestive disorders caused by SARS-CoV-2, we investigated the expression of ACE2 and TMPRSS2 proteins in the aerodigestive tracts of the tongue, hard palate with partial nasal tissue, larynx with hypopharynx, trachea, esophagus, lung, and kidney of rats through immunohistochemistry.ResultsStrong co-expression of ACE2 and TMPRSS2 proteins was observed in the nasal respiratory epithelium, trachea, bronchioles, alveoli, kidney, and taste buds of the tongue. Remarkably, TMPRSS2 expression was much stronger in the peripheral alveoli than in the central alveoli. These results coincide with the reported clinical symptoms of COVID-19, such as the loss of taste, loss of olfaction, respiratory dysfunction, and acute nephropathy.ConclusionsA wide range of organs have been speculated to be affected by SARS-CoV-2 depending on the expression levels of ACE2 and TMPRSS2. Differential distribution of TMPRSS2 in the lung indicated the COVID-19 symptoms to possibly be exacerbated by TMPRSS2 expression. This study might provide potential clues for further investigation of the pathogenesis of COVID-19.Level of EvidenceNA
Protozoa populations are ecosystem engineers that shape prokaryotic community structure and function of the rumen microbial ecosystem
Authors: Solomon Ronnie , Wein Tanita , Levy Bar , Eshed Shahar , Dror Rotem , Reiss Veronica , Zehavi Tamar , Furman Ori , Mizrahi Itzhak , Jami Elie 
Published: May 2020

AbstractUnicellular eukaryotes are an integral part of many microbial ecosystems communities where they are known to interact with their surrounding prokaryotic community – either as predators or as a mutualistic habitat. Within the rumen, one of the most complex host-associated microbial habitats, ciliate protozoa represent the main micro-eukaryotes, accounting for up to 50% of the microbial biomass. Nonetheless, the extent of the ecological effect of protozoa on the microbial community and on the rumen metabolic output remains largely understudied. To assess the role of protozoa on the rumen ecosystem, we established anex-vivosystem in which distinct protozoa sub-communities were introduced to native rumen prokaryotic community. We show that the different protozoa communities exert a strong and differential impact on the composition of the prokaryotic community, as well as its function including methane production. Furthermore, the presence of protozoa increases prokaryotic diversity with a differential effect on specific bacterial populations such as Gammaproteobacteria,Prevotellaand Spirochetes. Our results suggest that protozoa mitigate the effect of competitive exclusion between bacterial species, thereby contributing to the maintenance of prokaryotic diversity in the rumen. Our findings put forward the rumen protozoa populations as potentially important ecosystem engineers for future microbiome modulation strategies.
LC3B phosphorylation regulates FYCO1 binding and directional transport of autophagosomes
Authors: Nieto-Torres Jose L. , Shanahan Sean-Luc , Chassefeyre Romain , Landeras-Bueno Sara , Encalada Sandra E. , Hansen Malene 
Published: May 2020

SUMMARYMacroautophagy (hereafter referred to as autophagy) is a conserved process that promotes cellular homeostasis through the degradation of cytosolic components, also known as cargo. During autophagy, cargo is sequestered into double-membrane vesicles called autophagosomes, which are predominantly transported in the retrograde direction to the perinuclear region to fuse with lysosomes, thus ensuring cargo degradation [1]. The mechanisms regulating directional autophagosomal transport remain unclear. The ATG8 family of proteins associate with autophagosome membranes [2] and play key roles in autophagy, such as the movement of autophagosomes. This is achieved via the interaction of ATG8 with adaptor proteins, including FYCO1, a protein involved in the anterograde transport of autophagosomes toward the cell periphery [1,3–5]. We previously reported that phosphorylation of LC3B/ATG8 on threonine 50 (LC3B-T50) by the Hippo kinase STK4 is required for autophagy through unknown mechanisms [6]. Here, we show that LC3B-T50 phosphorylation decreases the interaction between LC3B and FYCO1, which in turn regulates the starvation-induced perinuclear positioning of autophagosomes. Moreover, non-phosphorylatable LC3B-T50A aberrantly switches the predominant retrograde movement of autophagosomes to anterograde movement towards the cell periphery in multiple cell types, including in mouse primary hippocampal neurons. Our data support a role of a nutrient-sensitive STK4–LC3B–FYCO1 axis in the regulation of the directional transport of autophagosomes via the post-translational regulation of LC3B. Given that autophagy is impaired in many human conditions, including neurodegenerative diseases, our findings may highlight new principles of vesicle transport regulation critical for disease etiology.Graphical abstract
A complex resistance locus inSolanum americanumrecognizes a conservedPhytophthoraeffector
Authors: Witek Kamil , Lin Xiao , Karki Hari S , Jupe Florian , Witek Agnieszka I , Steuernagel Burkhard , Stam Remco , van Oosterhout Cock , Fairhead Sebastian , Cocker Jonathan M , Bhanvadia Shivani , Barrett William , Wu Chih-Hang , Adachi Hiroaki , Song Tianqiao , Kamoun Sophien , Vleeshouwers Vivianne GAA , Tomlinson Laurence , Wulff Brande BH , Jones Jonathan DG 
Published: May 2020

AbstractLate blight caused byPhytophthora infestansgreatly constrains potato production. ManyResistance (R)genes were cloned from wildSolanumspecies and/or introduced into potato cultivars by breeding. However, individualRgenes have been overcome byP. infestansevolution; durable resistance remains elusive. We positionally cloned a newRgene,Rpi-amr1, fromSolanum americanum, that encodes an NRC helper-dependent CC-NLR protein.Rpi-amr1confers resistance in potato to all 19P. infestansisolates tested. Using association genomics and long-read RenSeq, we defined eight additionalRpi-amr1alleles from differentS. americanumand related species. Despite only ∼90% identity between Rpi-amr1 proteins, all confer late blight resistance but differentially recognizeAvramr1orthologs and paralogs. We propose thatRpi-amr1gene family diversity facilitates detection of diverse paralogs and alleles of the recognized effector, enabling broad-spectrum and durable resistance againstP. infestans.