bluuebunny/crossref_metadata_2025_split huggingface dataset:
Behavior-specific occupancy patterns of Pinyon Jays (Gymnorhinus cyanocephalus) in three Great Basin study areas and significance for pinyon-juniper woodland management
Authors: Boone John D. , Witt Chris , Ammon Elisabeth M. 
Published: August 2020

AbstractThe Pinyon Jay is a highly-social, year-round inhabitant of pinyon-juniper woodlands in the western United States. Range-wide, Pinyon Jays have declined ~ 3 – 4% per year for at least the last half-century. At the same time, large acreages of pinyon-juniper woodland have been removed or thinned to improve habitat for Greater Sage-Grouse or other game species across much of the Great Basin, which is home to nearly half of the global population of Pinyon Jays. Occupancy patterns and habitat use of Pinyon Jays have not been well characterized across much of the species’ range, and obtaining this information is necessary for better understanding the causes of ongoing declines and determining useful conservation strategies. Our goal of this study was to identify the characteristics of areas used by Pinyon Jays for several critical life history components and to thereby facilitate the inclusion of Pinyon Jay conservation measures in the design of vegetation management projects. To accomplish this, we studied Pinyon Jays in three widely separated study areas using radio telemetry and direct observation, and measured key attributes of their locations and a separate set of randomly-selected control sites using the U. S. Forest Service’s Forest Inventory Analysis protocol. Data visualizations, non-metric dimension scaling ordinations, and logistic regressions of the resulting data indicated that Pinyon Jay occupancy was concentrated in a distinct subset of available pinyon-juniper woodland habitat, and further that Pinyon Jays used different habitats, arrayed along elevational and tree-cover gradients, for seed caching, foraging, and nesting. Caching was concentrated in low-elevation, relatively flat areas with low tree cover; foraging occurred at slightly higher elevations with moderate tree cover, and nesting was concentrated in somewhat higher areas with greater tree cover and higher stand density. All three of these Pinyon Jay behavior types were highly concentrated within the lower-elevation band of pinyon-juniper woodland close to the woodland-shrubland ecotone. Because woodland removal projects in the Great Basin are often concentrated in these same areas, it is critical to incorporate conservation measures informed by Pinyon Jay occupancy patterns into existing woodland management paradigms, protocols, and practices.
Temperature alters gene expression in mosquitoes during arbovirus infection
Authors: Wimalasiri-Yapa BMC Randika , Barrero Roberto A. , Stassen Liesel , Hafner Louise M. , McGraw Elizabeth A. , Pyke Alyssa T. , Jansen Cassie C. , Suhrbier Andreas , Yakob Laith , Hu Wenbiao , Devine Gregor J. , Frentiu Francesca D. 
Published: August 2020

ABSTRACTArthropod-borne viruses (arboviruses) such as dengue, Zika and chikungunya constitute a significant proportion of the global disease burden. The principal vector of these pathogens is the mosquitoAedes(Ae.)aegypti, and its ability to transmit virus to a human host is influenced by environmental factors such as temperature. However, exactly how ambient temperature influences virus replication within mosquitoes remains poorly elucidated, particularly at the molecular level. Here, we use chikungunya virus (CHIKV) as a model to understand how the host mosquito transcriptome responds to arbovirus infection under different ambient temperatures. We exposed CHIKV-infected mosquitoes to 18 °C, 28 °C and 32 °C, and found higher temperature correlated with higher virus replication levels, particularly at early time points post-infection. Lower ambient temperatures resulted in reduced virus replication levels. Using RNAseq, we found that temperature significantly altered gene expression levels in mosquitoes, particularly components of the immune response. The highest number of significantly differentially expressed genes in response to CHIKV was observed at 28 °C, with a markedly more muted effect observed at either lower (18 °C) or higher (32 °C) temperatures. At the higher temperature, the expression of many classical immune genes, includingDicer-2in the RNAi pathway, was not substantially altered in response to CHIKV. Upregulation of Toll, IMD and JAK-STAT pathways was only observed at 28 °C. Time post infection also led to substantially different gene expression profiles, and this effect varied depending upon the which temperature mosquitoes were exposed to. Taken together, our data indicate temperature significantly modulates mosquito gene expression in response to infection, potentially leading to impairment of immune defences at higher ambient temperatures.
Fluorescent Nanosensors Reveal Dynamic pH Gradients During Biofilm Formation
Authors: Blunk Birte , Perkins Mark , Chauhan Veeren M. , Aylott Jonathan W. , Hardie Kim R. 
Published: August 2020

AbstractUnderstanding the dynamic environmental microniches of biofilms will permit us to detect, manage and exploit these communities. The components and architecture of biofilms have been interrogated in depth, however, little is known about the environmental microniches present. This is primarily because of the absence of tools with the required measurement sensitivity and resolution to detect these changes. We describe the application of ratiometric fluorescent pH-sensitive nanosensors, as a novel tool, to observe physiological pH changes in biofilms in real-time. Nanosensors comprised two pH-sensitive fluorophores covalently encapsulated with a reference pH-insensitive fluorophore in an inert polyacrylamide nanoparticle matrix. The nanosensors were used to analyse the real-time three-dimensional pH variation for two model biofilm formers: (i) opportunistic pathogenPseudomonas aeruginosa, and (ii) oral pathogenStreptococcus mutans. The detection of sugar metabolism in real time by nanosensors provides a potential application to identify novel therapeutic solutions to improve oral health.
Pharmacological inhibition of an epigenetic regulator during the formation of extinction memory reveals sensory cortical and subcortical codes for the specificity of salient cues
Authors: Rotondo Elena K. , Bieszczad Kasia M. 
Published: August 2020

ABSTRACTUsing a sound-reward extinction paradigm in male rats, we reveal both cortical and subcortical sensory codes for the cue-specificity of memory. In the auditory cortex, re-tuning narrowed frequency receptive field bandwidth, yielding more precise extinction behavior cued by acoustic frequency. Subcortical signals revealed in the auditory brainstem response (ABR) showed decreases in amplitude of select components of the ABR wave. Interestingly, treatment with an inhibitor of histone deacetylase 3 (HDAC3-i) facilitated both auditory cortical tuning bandwidth changes and ABR changes that were frequency-specific to the extinguished signal sound. Moreover, both changes were correlated to each other and with highly precise extinction memory at the level of behavior. Thus, we show for the first time that HDAC3 regulates the specificity of sensory features consolidated in extinction memory. Overall, the dynamics of auditory system plasticity associated with sound-specific extinction are complex. Changes in ABR amplitude induced by sound-reward learning disappeared after extinction, while changes in ABR slope that were initially induced by sound-reward learning were maintained through extinction. Moreover, plasticity of cortical re-tuning emerged only after extinction learning. HDAC3-i applied after extinction training sessions enabled sensory system plasticity to encode the extinguished sound with higher acoustic specificity (compared to vehicle controls). Both cortical and subcortical response changes to sound became unusually “tuned-in” to the acoustic frequency that had been presented under extinction conditions. Thus, HDAC3 regulates how specifically sensory features of experience are encoded into long-term memory and may exert its behavioral effects via multiple coding strategies along sensory system pathways.SIGNIFICANCE STATEMENTEpigenetic mechanisms have recently been implicated in memory and information processing. Here, we use a pharmacological inhibitor of histone deacetylase 3 (HDAC3) in a sensory model of learning to reveal, for the first time, its ability to enable unusually precise extinction memory. In so doing, we uncover neural coding strategies for memory’s “specificity” for sensory cues. Extinction induced multiple forms of change at different levels of sensory processing, which highlights the complexity of extinction memory encoding. HDAC3 appears to coordinate effects across sensory levels that determine specific cue saliency for behavior. Thus, epigenetic players may gate how sensory information is stored in long-term memory and their manipulation can be leveraged to reveal neural coding mechanisms for sensory detail in memory.
Repopulating Kupffer Cells Originate Directly from Hematopoietic Stem Cells
Authors: Fan Xu , Lu Pei , Cui Xianghua , Wu Peng , Lin Weiran , Zhang Dong , Yuan Shongzong , Liu Bing , Chen Fangyan , You Hong , Wei Handong , He Fuchu , Jia Jidong , Jiang Ying 
Published: August 2020

AbstractKupffer cells (KCs) originate from yolk sac progenitors before birth. Throughout adulthood, they self-maintain independently from the input of circulating monocytes (MOs) at stead state, and are replenished within 2 weeks after having been depleted, but the origin of repopulating KCs in adult remains unclear. The current paradigm dictates that repopulating KCs originate from preexisting KCs or monocytes, but there remains a lack of fate-mapping evidence. In current study, we firstly traced the fate of preexisting KCs and that of monocytic cells with tissue-resident macrophage-specific and monocytic cell-specific fate mapping mouse models, respectively, and found no evidences that repopulating KCs originate from preexisting KCs or MOs. Secondly, we performed genetic lineage tracing to determine the type of progenitor cells involved in response to KC depletion in mice, and found that in response to KC depletion, hematopoietic stem cells (HSCs) proliferated in the bone marrow, mobilized into the blood, adoptively transferred into the liver and differentiated into KCs. Finally, we traced the fate of HSCs in a HSC-specific fate-mapping mouse model, in context of chronic liver inflammation induced by repeated carbon tetrachloride treatment, and confirmed that repopulating KCs originated directly from HSCs. Taken together, these findings provided strong in vivo fate-mapping evidences that repopulating KCs originate directly from Hematopoietic stem cells not from preexisting KCs or from MOs.SignificanceThere is a standing controversy in the field regarding the cellular origin of repopulating macrophages. This paper provides strong in vivo fate-mapping evidences that repopulating KCs originate directly from hematopoietic stem cells not from preexisting KCs or from MOs, which presenting a completely novel understanding of the cellular origin of repopulating Kupffer Cells and shedding light on the divergent roles of KCs in liver homeostasis and diseases.
A novel isoform ofACE2is expressed in human nasal and bronchial respiratory epithelia and is upregulated in response to RNA respiratory virus infection
Authors: Blume Cornelia , Jackson Claire L , Spalluto Cosma Mirella , Legebeke Jelmer , Nazlamova Liliya , Conforti Franco , Perotin-Collard Jeanne-Marie , Frank Martin , Crispin Max , Coles Janice , Thompson James , Ridley Robert A , Dean Lareb S N , Loxham Matthew , Azim Adnan , Tariq Kamran , Johnston David , Skipp Paul J , Djukanovic Ratko , Baralle Diana , McCormick Chris , Davies Donna E , Lucas Jane S , Wheway Gabrielle , Mennella Vito 
Published: August 2020

AbstractAngiotensin-converting enzyme 2 (ACE2) is the main entry point in the airways for SARS-CoV-2. ACE2 binding to SARS-CoV-2 protein Spike triggers viral fusion with the cell membrane, resulting in viral RNA genome delivery into the host. Despite ACE2’s critical role in SARS-CoV-2 infection, an understanding of ACE2 expression, including in response to viral infection, remains unclear.Until nowACE2was thought to encode five transcripts and one 805 amino acid protein. Here we identify a novel short isoform of ACE2. ShortACE2is expressed in the airway epithelium, the main site of SARS-CoV-2 infection; it is substantially upregulated in response to interferon stimulation and RV infection, but not in response to SARS-CoV-2 infection, and it shows differential regulation in asthma patients. This short isoform lacks SARS-CoV-2 spike glycoprotein high-affinity binding sites and altogether, our data are consistent with a model where shortACE2may influence host susceptibility to SARS-CoV-2 infection.
Exacerbation of mitochondrial fission in human CD34+cells halts erythropoiesis and hemoglobin biosynthesis
Authors: Gonzalez-Ibanez Alvaro M. , Ruiz Lina M. , Jensen Erik , Echeverria Cesar A. , Romero Valentina , Stiles Linsey , Shirihai Orian , Elorza Alvaro A. 
Published: August 2020

AbstractErythropoiesis is the most powerful cellular differentiation and proliferation system, with a production of 1011cells per day. In this fine-tuned process, the hematopoietic stem cells (HSCs) generate erythroid progenitors, which proliferate and mature into erythrocytes. During erythropoiesis, mitochondria are reprogrammed to drive the differentiation process before finally being eliminated by mitophagy. In erythropoiesis, mitochondrial dynamics (MtDy) is expected to be a regulatory key point that has not been described previously. We described that a specific MtDy pattern is occurring in human erythropoiesis from EPO-induced human CD34+cells, characterized by a predominant mitochondrial fusion at early stages followed by predominant fission at late stages. The fusion protein MFN1 and the fission protein FIS1 are shown to play a key role in the accurate progression of erythropoiesis. Fragmentation of the mitochondrial web by the overexpression of FIS1 (gain of fission) resulted in both the inhibition of hemoglobin biosynthesis and the arrest of erythroid differentiation, keeping cells in immature differentiation stages. These cells showed specific mitochondrial features as compared with control cells, such as an increase in round and large mitochondria morphology, low mitochondrial membrane potential and a drop in the expression of the respiratory complexes II and IV. Interestingly, treatment with the mitochondrial permeability transition pore (mPTP) inhibitor cyclosporin A, rescued mitochondrial morphology, hemoglobin biosynthesis and erythropoiesis. Studies presented in this work revealed MtDy as a hot spot in the regulation of erythroid differentiation which might be signaling downstream for metabolic reprogramming through the aperture/close of the mPTP.Key Points-. Excessive fission disrupts erythroid progression, heme biosynthesis and mitochondrial function, keeping cells mostly in progenitors and proerythroblast stage.-. Mitochondrial Dynamics signaling for erythroid differentiation involves FIS1 and the mPTP
Transcript assembly improves expression quantification of transposable elements in single cell RNA-seq data
Authors: Shao Wanqing , Wang Ting 
Published: August 2020

AbstractTransposable elements (TEs) are an integral part of the host transcriptome. TE-containing noncoding RNAs (ncRNAs) exhibit considerable tissue specificity and play crucial roles during development, including stem cell maintenance and cell differentiation. Recent advances in single cell RNA-seq (scRNA-seq) revolutionized cell-type specific gene expression analysis. However, scRNA-seq quantification tools tailored for TEs are lacking, limiting our ability to dissect TE expression dynamics at single cell resolution. To address this issue, we established a TE expression quantification pipeline that is compatible with scRNA-seq data generated across multiple technology platforms. We constructed TE containing ncRNA references using bulk RNA-seq data and demonstrated that quantifying TE expression at the transcript level effectively reduces noise. As proof of principle, we applied this strategy to mouse embryonic stem cells and successfully captured the expression profile of endogenous retroviruses in single cells. We further expanded our analysis to scRNA-seq data from early stages of mouse embryogenesis. Our results illustrated the dynamic TE expression at pre-implantation stages and revealed 137 TE-containing ncRNA transcripts with substantial tissue specificity during gastrulation and early organogenesis.
SILAC proteomics implicates the ubiquitin conjugating enzyme UBE2D in SOCS1-mediated downmodulation of the MET receptor in hepatocytes
Authors: Santharam Madanraj Appiya , Shukla Akhil , Ihsan Awais Ullan , Cloutier Maryse , Levesque Dominique , Ramanathan Sheela , Boisvert François-Michel , Ilangumaran Subburaj 
Published: August 2020

AbstractSuppressor of Cytokine Signaling 1 (SOCS1) functions as a tumor suppressor in hepatocellular carcinoma (HCC) and many other types of cancers. SOCS1 mediates its functions by inhibiting tyrosine kinases, promoting ubiquitination and proteasomal degradation of signal transducing proteins, and by modulating transcription factors. Here, we studied the impact of SOCS1 on the hepatocyte proteome using Stable Isotopic Labelling of Amino acids in Cell culture (SILAC)-based mass spectrometry on the Hepa1-6 murine HCC cell line stably expressing wildtype SOCS1 or a mutant SOCS1 with impaired SH2 domain. As SOCS1 regulates the hepatocyte growth factor (HGF) receptor MET, the SILAC-labelled cells were stimulated or not with HGF. Following mass spectrometry analysis, differentially modulated proteins were identified, quantified and analyzed for pathway enrichment. Of the 3440 proteins identified in Hepa-SOCS1 cells at steady state, 181 proteins were significantly modulated compared to control cells. The SH2 domain mutation and HGF increased the number of differentially modulated proteins. Protein interaction network analysis revealed enrichment of SOCS1-modulated proteins within multiprotein complexes such as ubiquitin conjugating enzymes, proteasome, mRNA spliceosome, mRNA exosome and mitochondrial ribosome. These findings suggest that SOCS1, induced by cytokines, growth factors and diverse other stimuli, may dynamically modulate of large macromolecular regulatory complexes to help maintain cellular homeostasis. Notably, the expression of UBE2D ubiquitin conjugating enzyme, which is implicated in the control of growth factor receptor tyrosine kinase signaling, was found to be regulated by SOCS1.
Gut microbiota alterations due to fecal transplant
Authors: Olekhnovich Evgenii I. , Ivanov Artem B. , Ulyantsev Vladimir I. , Ilina Elena N. 
Published: August 2020

AbstractBackgroundFecal microbiota transplantation (FMT) is currently used to treat recurrent clostridial colitis and other diseases. However, neither the therapeutic mechanism of the FMT nor the mechanism that allows the donor bacteria to colonize the intestine of the recipient has yet been described. Moreover, FMT is a great model for studying the ecology of host-associated microbial communities. This creates the need for experimentation with approaches to metagenomic data analysis which may be useful to the interpretation of observed biological phenomena.MethodsHere the RECAST (Recipient intestinE Colonisation AnalysiS Tool) computational approach is presented, which is based on the shotgun reads sorting process in accordance with their origin in recipient metagenome. Using the RECAST algorithm, taxonomic/functional annotation, and machine learning, the shotgun metagenomic data from three FMT studies including healthy volunteers, patients with clostridial colitis and metabolic syndrome were analyzed.ResultsAccording to the analysis results, the colonizing and remaining microbial diversity in the post-FMT recipient metagenomic samples is clearly separated from the non-colonizers and lost. It is well explained by higher relative abundance in donor/pre-FMT recipient, Human Microbiome project metagenomes, and taxonomy. Moreover, the colonizing and remaining microbes are associated with lantibiotic and tetracyclines resistance genes.ConclusionBased on obtained results, the previously proposed “core” human gut microbiome concept may be elaborated. The top microbes of gut microbiota form “cores”, which, moreover, are mutually integrable between humans. Also, we assume that redistribution of microbial diversity in post-FMT recipients’ metagenomes is due to competition of donor/recipient microbes and to host immunity. The associations of top gut microbes with lantibiotic/antibiotic resistance can be related to gut microbiota colonization resistance phenomena or anthropogenic impact.
Retracing Schwann cell developmental transitions in embryonic dissociated DRG/Schwann cell cocultures in mice
Authors: Sundaram Venkat Krishnan , Jalkh Tatiana El , Barakat Rasha , Fernandez Camille Julie Isabelle , Massaad Charbel , Grenier Julien 
Published: August 2020

AbstractEmbryonic Dissociated Dorsal Root Ganglia cultures are often used to investigate the role of novel molecular pathways or drugs in Schwann cell development and myelination. These cultures largely recapitulate the order of cellular and molecular events that occur in Schwann cells of embryonic nerves. However, the timing of Schwann cell developmental transitions, notably the transition from Schwann Cell Precursors to immature Schwann cells and then to myelinating Schwann cells, has not been estimated so far in this culture system. In this study, we determined the expression profiles of Schwann cell developmental genes during the first week of culture and then compared our data to the expression profiles of these genes in developing spinal nerves. This helped in identifying that Schwann Cell Precursors transition into immature Schwann Cells between the 5thand 7thdayin vitro. Furthermore, we also investigated the transition of immature cells into pro-myelinating and myelinating Schwann cells upon the induction of myelinationin vitro. Our results suggest that Schwann cell differentiation beyond the immature stage can be observed as early as 4 days post the induction of myelination in cocultures. Finally, we compared the myelinating potential of coculture-derived Schwann cell monocultures to cultures established from neonatal sciatic nerves and found that both these cultures system exhibit similar myelinating phenotypes. In effect, our results allow for a better understanding and interpretation of coculture experiments especially in studies that aim to elucidate the role of a novel actor in Schwann Cell development and myelination.
Delta-band Cortical Tracking of Acoustic and Linguistic Features in Natural Spoken Narratives
Authors: Luo Cheng , Ding Nai 
Published: August 2020

AbstractSpeech contains rich acoustic and linguistic information. During speech comprehension, cortical activity tracks the acoustic envelope of speech. Recent studies also observe cortical tracking of higher-level linguistic units, such as words and phrases, using synthesized speech deprived of delta-band acoustic envelope. It remains unclear, however, how cortical activity jointly encodes the acoustic and linguistic information in natural speech. Here, we investigate the neural encoding of words and demonstrate that delta-band cortical activity tracks the rhythm of multi-syllabic words when naturally listening to narratives. Furthermore, by dissociating the word rhythm from acoustic envelope, we find cortical activity primarily tracks the word rhythm during speech comprehension. When listeners’ attention is diverted, however, neural tracking of words diminishes, and delta-band activity becomes phase locked to the acoustic envelope. These results suggest that large-scale cortical dynamics in the delta band are primarily coupled to the rhythm of linguistic units during natural speech comprehension.