bluuebunny/crossref_metadata_2025_split huggingface dataset:
Testosterone induces a female ornament followed by enhanced territoriality in a tropical songbird
Authors: Boersma Jordan , Enbody Erik D. , Jones John Anthony , Nason Doka , Lopez-Contreras Elisa , Karubian Jordan , Schwabl Hubert 
Published: April 2020

ABSTRACTWe know little of the proximate mechanisms underlying expression of signaling traits in female vertebrates. Across males the expression of sexual and competitive traits, including ornamentation and aggressive behavior, is often mediated by testosterone. In the White-shouldered Fairywren (Malurus alboscapulatus) of New Guinea, females of different subspecies differ in presence or absence of white shoulder patches and melanic plumage, while males are uniformly ornamented. Previous work has shown that ornamented females circulate more testosterone and exhibit more territorial aggression than do unornamented females. We investigated the degree to which testosterone regulates expression of ornamental plumage and territorial behavior by implanting free-living unornamented females with testosterone. Every testosterone-treated female produced a male-like cloacal protuberance, and 15 of 20 replaced plucked brown feathers with white shoulder patch feathers, but did not produce melanic plumage characteristic of ornamented females. Testosterone treatment did not elevate territorial behavior prior to production of the plumage ornament and exhaustion of the implant. However, females with experimentally induced ornamentation, but exhausted implants, increased the vocal components of territory defense relative to fully unornamented control and also to testosterone-implanted females. Our results suggest that testosterone induces partial acquisition of the ornamental plumage phenotype, and that ornament expression, rather than testosterone alone, results in elevated territorial behavior.Lay SummaryTestosterone regulates expression of a suite of competitive traits in male organisms and could have similar function in females. Empirical tests are needed to determine the extent to which testosterone promotes production of ornamentation and competitive behaviors in female animals. We supplemented testosterone in unornamented females of a species where naturally occurring ornamented females circulate higher testosterone and are more territorially aggressive. Implanted females produced partial ornamentation, which was followed by increased territoriality that was apparently unrelated to testosterone circulation itself.
Implications of back-and-forth motion and powerful propulsion for spirochetal invasion
Authors: Abe Keigo , Kuribayashi Toshiki , Takabe Kyosuke , Nakamura Shuichi 
Published: April 2020

AbstractThe spirocheteLeptospiraspp. can move in liquid and on a solid surface using two periplasmic flagella (PFs), and its motility is an essential virulence factor for the pathogenic species. Mammals are infected with the spirochete through the wounded dermis, which implies the importance of behaviors on the boundary with such viscoelastic milieu; however, the leptospiral pathogenicity involving motility remains unclear. We used a glass chamber containing a gel area adjoining the leptospiral suspension to resemble host dermis exposed to contaminated water and analyzed the motility of individual cells at the liquid-gel border. Insertion of one end of the cell body to the gel increased switching of the swimming direction. Moreover, the swimming force ofLeptospirawas also measured by trapping single cells using an optical tweezer. It was found that they can generate ∼17 pN of force, which is ∼30 times of the swimming force ofEscherichia coli. The force-speed relationship suggested the load-dependent force enhancement and showed that the power (the work per unit time) for the propulsion is ∼3.1×10−16W, which is two-order of magnitudes larger than the propulsive power ofE. coli. The powerful and efficient propulsion ofLeptospirausing back-and-forth movements could facilitate their invasion.
Safety, pharmacokinetics, and liver-stagePlasmodium cynomolgieffect of high-dose ivermectin and chloroquine in Rhesus Macaques
Authors: Vanachayangkul Pattaraporn , Im-erbsin Rawiwan , Tungtaeng Anchalee , Kodchakorn Chanikarn , Roth Alison , Adams John , Chaisatit Chaiyaporn , Saingam Piyaporn , Sciotti Richard J. , Reichard Gregory A. , Nolan Christina K. , Pybus Brandon S. , Black Chad C. , Lugo Luis A. , Wegner Matthew D. , Smith Philip L. , Wojnarski Mariusz , Vesely Brian A. , Kobylinski Kevin C. 
Published: April 2020

AbstractPreviously, ivermectin (1–10 mg/kg) was shown to inhibit liver-stage development ofPlasmodium bergheiin orally dosed mice. Here, ivermectin showed inhibition of thein vitrodevelopment ofPlasmodium cynomolgischizonts (IC50= 10.42 μM) and hypnozoites (IC50= 29.24 μM) in primary macaque hepatocytes when administered in high-dose prophylactically but not when administered in radical cure mode. The safety, pharmacokinetics, and efficacy of oral ivermectin (0.3, 0.6, and 1.2 mg/kg) with and without chloroquine (10 mg/kg) administered for seven consecutive days was evaluated for prophylaxis or radical cure ofPlasmodium cynomolgiliver-stages in Rhesus macaques. No inhibition or delay to blood-stageP. cynomolgiparasitemia was observed at any ivermectin dose (0.3, 0.6, and 1.2 mg/kg). Ivermectin (0.6 and 1.2 mg/kg) and chloroquine (10 mg/kg) in combination were well-tolerated with no adverse events and no significant pharmacokinetic drug-drug interactions observed. Repeated daily ivermectin administration for seven days did not inhibit ivermectin bioavailability. It was recently demonstrated that both ivermectin and chloroquine inhibit replication of the novel Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2)in vitro. Further ivermectin and chloroquine trials in humans are warranted to evaluate their role inPlasmodium vivaxcontrol and as adjunctive therapies against COVID-19 infections.
Loss of the extracellular matrix molecule tenascin-C leads to absence of reactive gliosis and promotes anti-inflammatory cytokine expression in an autoimmune glaucoma mouse model
Authors: Wiemann Susanne , Reinhard Jacqueline , Reinehr Sabrina , Cibir Zülal , Joachim Stephanie C. , Faissner Andreas 
Published: April 2020

AbstractPrevious studies demonstrated that retinal damage correlates with a massive remodeling of extracellular matrix (ECM) molecules and reactive gliosis. However, the functional significance of the ECM in retinal neurodegeneration is still unknown. In the present study, we used an intraocular pressure (IOP) independent experimental autoimmune glaucoma (EAG) mouse model to examine the role of the ECM glycoprotein tenascin-C (Tnc).Wild type (WT ONA) and Tnc knockout (KO ONA) mice were immunized with an optic nerve antigen (ONA) homogenate and control groups (CO) obtained sodium chloride (WT CO, KO CO). IOP was measured weekly and electroretinographies were recorded at the end of the study. 10 weeks after immunization, we analyzed retinal ganglion cells (RGCs), glial cells and the expression of different cytokines in retina and optic nerve tissue in all four groups.IOP and retinal function was comparable in all groups. Although less severe in KO ONA, WT and KO mice displayed a significant loss of RGCs after immunization. Compared to KO ONA, a significant reduction of βIII-tubulin stained axons and oligodendrocyte markers was noted in the optic nerve of WT ONA. In retinal and optic nerve slices, we found an enhanced GFAP+staining area of astrocytes in immunized WT. In retinal flat-mounts, a significantly higher number of Iba1+microglia was found in WT ONA, while a lower number of Iba1+cells was observed in KO ONA. Furthermore, an increased expression of the glial markersGfap, Iba1, Nos2andCd68was detected in retinal and optic nerve tissue of WT ONA, whereas comparable levels were observed in KO ONA post immunization. In addition, pro-inflammatoryTnfaexpression was upregulated in WT ONA, but downregulated in KO ONA. Vice versa, a significantly increased anti-inflammatoryTgfbexpression was measured in KO ONA animals.Collectively, this study revealed that Tnc plays an important role in glial and inflammatory response during retinal neurodegeneration. Our results provide evidence that Tnc is involved in glaucomatous damage by regulating retinal glial activation and cytokine release. Thus, this transgenic EAG mouse model offers for the first time the possibility to investigate IOP-independent glaucomatous damage in direct relation to ECM remodeling.
Bistability in oxidative stress response determines the migration behavior of phytoplankton in turbulence
Authors: Carrara Francesco , Sengupta Anupam , Behrendt Lars , Vardi Assaf , Stocker Roman 
Published: April 2020

AbstractTurbulence is an important determinant of phytoplankton physiology, often leading to cell stress and damage. Turbulence affects phytoplankton migration, both by transporting cells and by triggering switches in migratory behavior, whereby vertically migrating cells can invert their direction of migration upon exposure to turbulent cues. However, a mechanistic link between single-cell physiology and vertical migration of phytoplankton in turbulence is currently missing. Here, by combining physiological and behavioral experiments with a mathematical model of stress accumulation and dissipation, we show that the mechanism responsible for the switch in the direction of migration in the marine raphidophyteHeterosigma akashiwois the integration of reactive oxygen species (ROS) signaling generated by turbulent cues. Within timescales as short as tens of seconds, the emergent downward-migrating subpopulation exhibited a two-fold increase of ROS, an indicator of stress, 15% lower photosynthetic efficiency, and 35% lower growth rate over multiple generations compared to the upward-migrating subpopulation. The origin of the behavioral split in a bistable oxidative stress response is corroborated by the observation that exposure of cells to exogenous stressors (H2O2, UV-A radiation or high irradiance), in lieu of turbulence, caused comparable ROS accumulation and an equivalent split into the two subpopulations. By providing a mechanistic link between single-cell physiology, population-scale migration and fitness, these results contribute to our understanding of phytoplankton community composition in future ocean conditions.Significance StatementTurbulence has long been known to drive phytoplankton fitness and species succession: motile species dominate in calmer environments and non-motile species in turbulent conditions. Yet, a mechanistic understanding of the effect of turbulence on phytoplankton migratory behavior and physiology is lacking. By combining a method to generate turbulent cues, quantification of stress accumulation and physiology, and a mathematical model of stress dynamics, we show that motile phytoplankton use their mechanical stability to sense the intensity of turbulent cues and integrate these cues in time via stress signaling to trigger switches in migratory behavior. The stress-mediated warning strategy we discovered provides a paradigm for how phytoplankton cope with turbulence, thereby potentially governing which species will be successful in a changing ocean.
Self-reported sleep problems are related to cortical thinning in aging but not memory decline and amyloid-β accumulation – results from the Lifebrain consortium
Authors: Fjell Anders M. , Sørensen Øystein , Amlien Inge K. , Bartrés-Faz David , Brandmaier Andreas M. , Buchmann Nikolaus , Demuth Ilja , Drevon Christian A , Düzel Sandra , Ebmeier Klaus P. , Ghisletta Paolo , Idland Ane-Victoria , Kietzmann Tim C. , Kievit Rogier A. , Kühn Simone , Lindenberger Ulman , Magnussen Fredrik , Macià Didac , Mowinckel Athanasia M. , Nyberg Lars , Sexton Claire E. , Solé-Padullés Cristina , Pudas Sara , Roe James M. , Sederevicius Donatas , Suri Sana , Vidal-Piñeiro Didac , Wagner Gerd , Watne Leiv Otto , Westerhausen René , Zsoldos Enikő , Walhovd Kristine B. ,   for the Alzheimer’s Disease Neuroimaging Initiative
Published: April 2020

AbstractBackgroundOlder persons with poor sleep are more likely to develop neurodegenerative disease, but the causality underlying this association is unclear. To move towards explanation, we examine whether sleep quality and quantity are similarly associated with brain changes across the adult lifespan.MethodsAssociations between self-reported sleep parameters (Pittsburgh Sleep Quality Index;PSQI) and longitudinal cortical change were tested using five samples from theLifebrainconsortium (n=2205, 4363 MRIs, 18-92 years). Analyses were augmented by considering episodic memory change, gene expression from the Allen Human Brain Atlas, and amyloid-beta (Aβ) accumulation (n=1980).ResultsPSQI components sleep problems and low sleep quality were related to thinning of the right lateral temporal cortex. The association with sleep problems emerged after 60 years, especially in regions with high expression of genes related to oligodendrocytes and S1 pyramidal neurons. BMI and symptoms of depression had negligible effects. Sleep problems were neither related to longitudinal change in episodic memory function nor to Aβ accumulation, suggesting that sleep-related cortical changes were independent of AD neuropathology and cognitive decline.ConclusionWorse self-reported sleep in later adulthood was associated with more cortical thinning in regions of high expression of genes related to oligodendrocytes and S1 pyramidal neurons, but not to Aβ accumulation or memory decline. The relationship to cortical brain change suggests that self-reported sleep parameters are relevant in lifespan studies, but small effect sizes, except for a few restricted regions, indicate that self-reported sleep is not a good biomarker of general cortical degeneration in healthy older adults.
GeneTEFlow: A Nextflow-based pipeline for analysing gene and transposable elements expression from RNA-Seq data
Authors: Liu Xiaochuan , Bienkowska Jadwiga R , Zhong Wenyan 
Published: April 2020

AbstractTransposable elements (TEs) are mobile genetic elements in eukaryotic genomes. Recent research highlights the important role of TEs in the embryogenesis, neurodevelopment, and immune functions. However, there is a lack of a one-stop and easy to use computational pipeline for expression analysis of both genes and locus-specific TEs from RNA-Seq data. Here, we present GeneTEFlow, a fully automated, reproducible and platform-independent workflow, for the comprehensive analysis of gene and locus-specific TEs expression from RNA-Seq data employing Nextflow and Docker technologies. This application will help researchers more easily perform integrated analysis of both gene and TEs expression, leading to a better understanding of roles of gene and TEs regulation in human diseases. GeneTEFlow is freely available athttps://github.com/zhongw2/GeneTEFlow.
Mosquito defensins enhance Japanese encephalitis virus infection by facilitating virus adsorption and entry within mosquito
Authors: Liu Ke , Xiao Changguang , Xi Shumin , hameed Muddassar , Wahaab Abdul , Shao Donghua , Li Zongjie , Li Beibei , Wei Jianchao , Qiu Yafeng , Miao Denian , Zhu Huaimin , Ma Zhiyong 
Published: April 2020

AbstractJapanese encephalitis virus (JEV) is a viral zoonosis which can cause viral encephalitis, death and disability.Culexis the main vector of JEV, but little is known about JEV transmission by this kind of mosquito. Here, we found that mosquito defensin facilitated the adsorption of JEV on target cells via both direct and indirect pathways. Mosquito defensin bound the ED III domain of viral E protein and directly mediated efficient virus adsorption on the target cell surface, Lipoprotein receptor-related protein 2 expressed on the cell surface is the receptor affecting defensin dependent adsorption. Mosquito defensin also indirectly down-regulated the expression of an antiviral protein, HSC70B. As a result, mosquitos defensin enhances JEV infection in salivary gland while increasing the possibility of viral transmission by mosquito. These findings demonstrate that the novel effects of mosquito defensin in JEV infection and the mechanisms through which the virus exploits mosquito defensin for infection and transmission.
Extensive 5’-Surveillance Guards Against Non-Canonical NAD-Caps of Nuclear mRNAs in Yeast
Authors: Zhang Yaqing , Kuster David , Schmidt Tobias , Kirrmaier Daniel , Nübel Gabriele , Ibberson David , Benes Vladimir , Hombauer Hans , Knop Michael , Jäschke Andres 
Published: April 2020

SummaryThe ubiquitous redox coenzyme nicotinamide adenine dinucleotide (NAD) acts as a non-canonical cap structure on prokaryotic and eukaryotic ribonucleic acids. Here we find that in budding yeast, NAD-RNAs are abundant (>1400 species), short (<170 nt), and mostly correspond to mRNA 5’-ends. The modification percentage is low (<5%). NAD is incorporated during the initiation step by RNA polymerase II, which uses distinct promoters with a YAAG core motif for this purpose. Most NAD-RNAs are 3’-truncated. At least three decapping enzymes, Rai1, Dxo1, and Npy1, guard against NAD-RNA at different cellular locations, targeting overlapping transcript populations. NAD-mRNAs do not support translationin vitro. Our work indicates that in budding yeast, most of the NAD incorporation into RNA seems to be accidental and undesirable to the cell, which has evolved a diverse surveillance machinery to prematurely terminate, decap and reject NAD-RNAs.In BriefIn budding yeast, most of the NAD incorporation into RNA seems to be accidental and undesirable to the cell, which has evolved a diverse surveillance machinery to prematurely terminate, decap and reject NAD-RNAs.Graphical AbstractHighlightsYeast cells have thousands of short NAD-RNAs related to the 5’-ends of mRNAsRNA polymerase II prefers a YAAG promoter motif for NAD incorporation into RNANAD-RNA is strongly guarded against by Rai1, Dxo1, and Npy1 decapping enzymes at different subcellular sitesIn vitro, NAD-mRNAs are rejected from translation
MicroRNA composition delineates cardiosphere-derived cell and mesenchymal stem cell extracellular vesicles
Authors: Walravens Ann-Sophie , Smolgovsky Sasha , Li Liang , Kelly Lauren , Antes Travis , Peck Kiel , Quon Tanner , Marbán Linda , Berman Benjamin , -Borlado Luis R. , de Couto Geoffrey 
Published: April 2020

AbstractCell therapy limits ischemic injury following myocardial infarction (MI) by limiting cell death, modulating the immune response, and promoting tissue regeneration. The therapeutic efficacy of cardiosphere-derived cells (CDCs) and mesenchymal stem cells (MSCs) is associated with extracellular vesicle (EV) release. Despite differences in cell origin, it is unclear why EVs elicit differences in therapeutic potency between cell types. Here, we compare EVs derived from multiple MSC and CDC donors. We reveal that EV membrane protein and microRNA (miR) composition are reflective of their parent cell. Small RNA-sequencing revealed enrichment of miR-10b in MSC EVs. Our data support the hypothesis that CDC EVs are distinct from MSC-EVs and is reflected by their miR composition.
Field-deployable molecular diagnostic platform for arbovirus andWolbachiadetection inAedes aegypti
Authors: Rutkowski Natalie N. , Dong Yuemei , Dimopoulos George 
Published: April 2020

AbstractBackgroundSurveillance of mosquito infection status is critical for planning and deployment of proper mosquito control initiatives. Concurrently,Wolbachiais being widely used as a control method for arboviral transmission. Point-of-care (POC) detection assays are necessary for monitoring the infection prevalence and geographic range of viruses as well asWolbachiain mosquito vector populations. We therefore assessed the novel qPCR bCUBE molecular diagnostic system as a tool for virus andWolbachiadetection.ResultsWe developed a reliable, specific, and sensitive diagnostic assay for detecting Zika virus and dengue virus serotype 2 using the real-time qPCR platform bCUBE. With bCUBE-based qRT-PCR, bothWolbachiabacterium and virus RNA could be reliably detected in individually infectedAe. aegyptimosquitoes and in pools of 5, 10, or 15 mosquitoes.ConclusionsThe portable qPCR bCUBE diagnostic platform is capable of detecting Zika and dengue virus as well asWolbachiain mosquitoes and therefore has potential as a practical field-deployable diagnostic test for vector-borne disease surveillance programs.
Using Expansion Microscopy to visualize and characterize the morphology of mitochondrial cristae
Authors: Kunz Tobias C. , Götz Ralph , Gao Shiqiang , Sauer Markus , Kozjak-Pavlovic Vera 
Published: April 2020

AbstractMitochondria are double membrane bound organelles indispensable for biological processes such as apoptosis, cell signalling, and the production of many important metabolites, which includes ATP that is generated during the process known as oxidative phosphorylation (OXPHOS). The inner membrane contains folds called cristae, which increase the membrane surface and thus the amount of membrane-bound proteins necessary for the OXPHOS. These folds have been of great interest not only because of their importance for energy conversion, but also because changes in morphology have been linked to a broad range of diseases from cancer, diabetes, neurodegenerative diseases, to ageing and infection. With a distance between opposing cristae membranes often below 100 nm, conventional fluorescence imaging cannot provide a resolution sufficient for resolving these structures. For this reason, various highly specialized super-resolution methods includingdSTORM, PALM, STED and SIM have been applied for cristae visualisation.Expansion Microscopy (ExM) offers the possibility to perform super-resolution microscopy on conventional confocal microscopes by embedding the sample into a swellable hydrogel that is isotropically expanded by a factor of 4-4.5, improving the resolution to 60-70 nm on conventional confocal microscopes, which can be further increased to ∼ 30 nm laterally using SIM. Here, we demonstrate that the expression of the mitochondrial creatine kinase MtCK linked to marker protein GFP (MtCK-GFP), which localizes to the space between the outer and the inner mitochondrial membrane, can be used as a cristae marker. Applying ExM on mitochondria labelled with this construct enables visualization of morphological changes of cristae and localization studies of mitochondrial proteins relative to cristae without the need for specialized setups. For the first time we present the combination of specific mitochondrial intermembrane space labelling and ExM as a tool for studying internal structure of mitochondria.
Mammalian SWI/SNF chromatin remodeler is essential for reductional meiosis in males
Authors: Menon Debashish U. , Magnuson Terry 
Published: April 2020

AbstractBRG1, a catalytic subunit of the mammalian SWI/SNF nucleosome remodeler is essential for male meiosis1. In addition to BRG1, multiple subunits (~10-14) some of which are mutually exclusive, constitute biochemically distinct SWI/SNF subcomplexes, whose functions in gametogenesis remain unknown. Here, we identify a role for the PBAF (Polybromo- Brg1AssociatedFactor) complex in the regulation of meiotic cell division. The germ cell-specific depletion of PBAF specific subunit, ARID2 resulted in a metaphase-I arrest.Arid2cKOmetaphase-I spermatocytes displayed defects in chromosome organization and spindle assembly. Additionally, mutant centromeres were devoid of Polo-like kinase1 (PLK1), a known regulator of the spindle assembly checkpoint (SAC)2. The loss of PLK1 coincided with an abnormal chromosome-wide expansion of centromeric chromatin modifications such as Histone H3 threonine3 phosphorylation (H3T3P) and Histone H2A threonine120 phosphorylation (H2AT120P) that are critical for chromosome segregation3,4. Consistent with the known role of these histone modifications in chromosome passenger complex (CPC) recruitment,Arid2cKOmetaphase-I chromosomes display defects in CPC association. We propose that ARID2 facilitates metaphase-I exit by regulating spindle assembly and centromeric chromatin.