bluuebunny/crossref_metadata_2025_split huggingface dataset:
Dynamic changes in gas solubility of xylem sap reiterate the enigma of plant water transport under negative pressure
Authors: Pereira Luciano , Jansen Steven , Miranda Marcela T. , Pacheco Vinícius S. , Kaack Lucian , Pires Gabriel S. , Guan Xinyi , Mayer Juliana L.S. , Machado Eduardo C. , Schenk H. Jochen , Ribeiro Rafael V. 
Published: January 2022

AbstractDespite a long research history, we do not fully understand why plants are able to transport xylem sap under negative pressure without constant failure. Microbubble formation via direct gas entry is assumed to cause hydraulic failure, while the concentration of gas dissolved in xylem sap is traditionally supposed to be constant, following Henry’s law. Here, the concentration of soluble gas in xylem sap was estimatedin vivousing well-wateredCitrusplants under varying levels of air temperature and photoperiodic exposure, and compared to modelled data. The gas concentration in xylem sap showed non-equilibrium curves, with a minimum over- or undersaturation of 5% compared to gas solubility based on Henry’s law. A similar diurnal pattern was obtained from the gas concentration in the cut-open conduits and discharge tube, and oversolubility was strongly associated with decreasing xylem water potentials during transpiration. Although our model did not explain the daily changes in gas solubility for an anisobaric situation, oversolubility characterises nanoconfined liquids, such as sap inside cell walls. Thus, plants are able to transport sap under negative pressure with relatively high amounts of dissolved gas, providing them with a buffering capacity to prevent hydraulic failure, despite diurnal changes in pressure and temperature.
Genome-wide SNPs of vegetable leafminer, Liriomyza sativae: insights into the recent Australian invasion
Authors: Xu Xuefen , Schmidt Tom L. , Liang Jiaxin , Ridland Peter M. , Chung Jessica , Yang Qiong , Jasper Moshe , Umina Paul A. , Hoffmann Ary A. 
Published: January 2022

AbstractLiriomyza sativae, the vegetable leafminer, is a serious agricultural pest originally from the Americas which has now colonized all continents except Antarctica. In 2015, L. sativae arrived on the Australian mainland and established on the Cape York Peninsula in the northeast of the country. Here, we assessed genetic variation in L. sativae based on genome-wide single nucleotide polymorphisms (SNPs) generated by double-digest restriction-site associated DNA sequencing (ddRAD-seq) to uncover the potential origin(s) of this pest in Australia and contribute to reconstructing its global invasion history. Our principal component analyses (PCA) results suggested that Australian mainland populations were genetically close to populations from the Torres Strait and had connections to Bali and Papua New Guinea (PNG), whereas populations from Asia and Africa were more distantly related. Hawaii was genetically distinct from populations from Asia, Africa and Australia. Co-ancestry analyses pointed to signals of gene flow from the Torres Strait into the Australian mainland, while Indonesia/PNG were the likely sources of the initial invasion into the Torres Strait. Admixture analyses further revealed that L. sativae from the Torres Strait had genetic diversity originating from multiple sources, which has now spread to the Australian mainland. The L. sativae lineages from Asia/Africa appear closely related and may share co-ancestry. Isolation by distance (IBD) was found at a broad global scale, but not within small regions, suggesting human-mediated factors contribute to the local spread of this pest. Overall, our findings highlight the challenges in quarantine measures aimed at restricting the distribution of this global pest.
Regulation of major bacterial survival strategies by transcript sequestration in a membraneless organelle
Authors: Szoke Tamar , Albocher Nitsan , Goldberger Omer , Barsheshet Meshi , Nussbaum-Shochat Anat , Wiener Reuven , Schuldiner Maya , Amster-Choder Orna 
Published: January 2022

ABSTRACTLiquid-liquid phase separation (LLPS) of proteins was shown in recent years to regulate spatial organization of cell content without the need for membrane encapsulation in eukaryotes and prokaryotes. Yet evidence for the relevance of LLPS for bacterial cell functionality is largely missing. Here we show that the sugar metabolism-regulating clusters, recently shown by us to assemble in theE. colicell poles by means of the novel protein TmaR, are formed via LLPS. A mutant screen uncovered residues and motifs in TmaR that are important for its condensation. Upon overexpression, TmaR undergoes irreversible liquid-to-solid transition, similar to the transition of disease-causing proteins in human, which impairs bacterial cell morphology and proliferation. Not only does RNA contribute to TmaR phase separation, but by ensuring polar localization and stability of flagella-related transcripts, TmaR enables cell motility and biofilm formation, thus providing a linkage between LLPS and major survival strategies in bacteria.
Sperm exposure to accessory gland secretions alters the transcriptomic response of the endometrium in cattle
Authors: Sánchez José María , Rabaglino María Belén , Bagés-Arnal Sandra , McDonald Michael , Behura Susanta K , Spencer Thomas E , Lonergan Pat , Fernandez-Fuertes Beatriz 
Published: January 2022

ABSTRACTIn a recent study from our group, mating to intact, but not vasectomised, bulls modified the endometrial transcriptome, suggesting an important role of sperm in the modulation of the uterine environment in this species. However, it is not clear whether these changes are driven by intrinsic sperm factors, or by factors of accessory gland (AG) origin that bind to sperm at ejaculation. Thus, the aim of the present study was to determine whether ejaculated sperm, which are suspended in the secretions of the AGs, elicit a different endometrial transcriptomic response than epididymal sperm, which have never been exposed to AG factors. To this end, bovine endometrial explants collected from heifers in oestrus were incubated alone (control), or with epididymal or ejaculated sperm. RNA-sequencing revealed 1912 differentially expressed genes (DEGs) between in endometrial explants exposed to epididymal sperm compared with control explants, whereas 115 DEGs genes detected between endometrial explants exposed to ejaculated sperm in comparison to control explants. In both cases, the top pathways associated with these genes included T cell regulation and NF-KB and IL17 signalling. To confirm whether AG factors were directly responsible for the dampening of the endometrial response elicited by ejaculated sperm, endometrial explants were incubated with epididymal sperm previously exposed, or not, to seminal plasma (SP). Exposure to SP abrogated the downregulation of SQSTM1 by epididymal sperm, and partially inhibited the upregulation of MYL4 and CHRM3 and downregulation of SCRIB. These data indicate that factors of AG origin modulate the interaction between sperm and the endometrium in cattle.
Multiomic analisys reveals that viroid infection induces a temporal reprograming of plant-defence mechanisms at multiple regulatory levels
Authors: Márquez-Molins Joan , Villalba-Bermell Pascual , Corell-Sierra Julia , Pallás Vicente , Gómez Gustavo 
Published: January 2022

ABSTRACTViroids are circular RNAs of minimal complexity compelled to subvert plant-regulatory networks to accomplish their infectious process. Studies focused on the response to viroid infection have mostly addressed specific regulatory levels and considered a unique infection time. Thus, much remains to be done to understand the temporal evolution and complex nature of viroid-host interactions. Here we present an integrative analysis of the temporal evolution and intensity of the genome-wide alterations in cucumber plants infected with hop stunt viroid (HSVd) by integrating differential host transcriptome, sRNAnome and methylome. Our results support that HSVd promotes the redesign of the cucumber regulatory-pathways predominantly affecting specific regulatory layers at different infection-phases. The initial response was characterized by a reconfiguration of the host-transcriptome by differential exon usage, followed by a progressive transcriptional down-regulation modulated by epigenetic changes. Regarding endogenous small RNAs, the alterations were limited and mainly occur at the late stage. The most significant host-alterations were predominantly related to the down-regulation of transcripts involved in plant-defence mechanisms, the restriction of pathogen-movement and the systemic spreading of defence signals. Altogether our data evidence the existence of a dynamic and yet poorly known arms race between the host and the viroid. We expect that these data constituting the first comprehensive map of the plant responses to a viroid infection contribute to elucidate the molecular basis of this multifaceted defence and counter-defence layout.
Neural correlate of reduced respiratory chemosensitivity during chronic epilepsy
Authors: Bhandare Amol , Dale Nicholas 
Published: January 2022

AbstractCentral autonomic cardiorespiratory dysfunction underlies sudden unexpected death in epilepsy (SUDEP). Here we used single cell neuronal Ca2+imaging and intrahippocampal kainic acid (KA)-induced chronic epilepsy in mice to investigate progressive changes in key cardiorespiratory brainstem circuits during chronic epilepsy. Following induction of status epilepticus (SE), adaptive ventilatory responses to hypercapnia were reduced in mice with chronic epilepsy for 5 weeks post-SE with partial recovery at week 7. These changes were paralleled by post-SE alterations in the chemosensory responses of neurons in the retrotrapezoid nucleus (RTN). Neurons that displayed adapting responses to hypercapnia were less prevalent and exhibited smaller responses over weeks 3-5, whereas neurons that displayed graded responses to hypercapnia became more prevalent by week 7. Over the same period, chemosensory responses of the presympathetic rostral ventrolateral medullary neurons showed no change. Mice with chronic epilepsy showed enhanced sensitivity to seizures, which can invade the RTN and possibly impair further the chemosensory circuits. Our work suggests that assessment of respiratory chemosensitivity may have potential for identifying people at risk of SUDEP.
Validation that human microbiome phages use alternative genetic coding with TAG stop read as Q
Authors: Peters Samantha L. , Borges Adair L. , Giannone Richard J. , Morowitz Michael J. , Banfield Jillian F. , Hettich Robert L. 
Published: January 2022

AbstractMetagenomic findings suggesting that bacteriophages (phages) can use genetic codes different from those of their host bacteria reveal a new dimension of phage-host interaction dynamics. Whereas reassignment of stop codons to code for amino acids has been predicted, there has been no proteomic validation of alternative coding in phages. In fact, one code where the stop codon TAG is reassigned to glutamine (code 15) has never been experimentally validated in any biological system. Here, we characterized stop codon reassignment in two crAss-like phages found in the human gut microbiome using LC-MS/MS-based metaproteomics. The proteome data from several phage structural proteins clearly demonstrates reassignment of the TAG stop codon to glutamine, establishing for the first time the expression of genetic code 15.One-Sentence SummaryMass spectrometry confirms protein expression of predicted alternate genetic coding in phage genomes from human microbiomes.
Feasibility of Using Wearable EMG Armbands combined with Unsupervised Transfer Learning for Seamless Myoelectric Control
Authors: Sohn M. Hongchul , Lai Sonia Yuxiao , Elwin Matthew L. , Dewald Julius P.A. 
Published: January 2022

ABSTRACTMyoelectric control uses electromyography (EMG) signals as human-originated input to enable intuitive interfaces with machines. As such, recent rehabilitation robotics employs myoelectric control to autonomously classify user intent or operation mode using machine learning. However, performance in such applications inherently suffers from the non-stationarity of EMG signals across measurement conditions. Current laboratory-based solutions rely on careful, time-consuming control of the recordings or periodic recalibration, impeding real-world deployment. We propose that robust yet seamless myoelectric control can be achieved using a low-end, easy-to-“don” and “doff” wearable EMG sensor combined with unsupervised transfer learning. Here, we test the feasibility of one such application using a consumer-grade sensor (Myo armband, 8 EMG channels @ 200 Hz) for gesture classification across measurement conditions using an existing dataset: 5 users x 10 days x 3 sensor locations. Specifically, we first train a deep neural network using Temporal-Spatial Descriptors (TSD) with labeled source data from any particular user, day, or location. We then apply the Self-Calibrating Asynchronous Domain Adversarial Neural Network (SCADANN), which automatically adjusts the trained TSD to improve classification performance for unlabeled target data from a different user, day, or sensor location. Compared to the original TSD, SCADANN improves accuracy by 12±5.2% (avg±sd), 9.6±5.0%, and 8.6±3.3% across all possible user-to-user, day-to-day, and location-to-location cases, respectively. In one best-case scenario, accuracy improves by 26% (from 67% to 93%), whereas sometimes the gain is modest (e.g., from 76% to 78%). We also show that the performance of transfer learning can be improved by using a “better” model trained with “good” (e.g., incremental) source data. We postulate that the proposed approach is feasible and promising and can be further tailored for seamless myoelectric control of powered prosthetics or exoskeletons.
The principal mitochondrial K+ uniport is associated with respiratory complex I
Authors: Zemel Michael , Angelin Alessia , Potluri Prasanth , Wallace Douglas C. , Fieni Francesca 
Published: January 2022

This manuscript has been withdrawn by the authors due to disagreement with UCSF over data rights.This withdrawal decision is not related to the validity of the data presented in this study, and these authors understand that this work cannot be cited as reference for the project until the disagreement is resolved.
Moment-Based Estimation of State-Switching Rates in Cell Populations
Authors: Saint-Antoine Michael , Singh Abhyudai 
Published: January 2022

AbstractIn isogenic cell populations, cells can switch back and forth between different gene expression states. These expression states can be biologically relevant. For example, a certain expression state may cause a tumor cell to be resistant to treatment, while another state may leave it vulnerable to treatment. However, estimating the rates of state-switching can be difficult, because experimentally measuring a cell’s transcriptome often involves destroying the cell, so it can only be measured once. In this paper, we propose a computational method to estimate the rate of switching between expression states, given data from a Luria-Delbrück style fluctuation test that is experimentally simple and feasible. We then benchmark this method using simulated data to test its efficacy, with varying assumptions made about cell cycle timing distribution in the simulations.
Target binding triggers hierarchical phosphorylation of human Argonaute-2 to promote target release
Authors: Bibel Brianna , Elkayam Elad , Silletti Steve , Komives Elizabeth A , Joshua-Tor Leemor 
Published: January 2022

AbstractArgonaute (Ago) proteins play a central role in post-transcriptional gene regulation through RNA interference (RNAi). Agos bind small RNAs (sRNAs) including small interfering RNAs (siRNAs) and microRNAs (miRNAs) to form the functional core of the RNA Induced Silencing Complex (RISC). The sRNA is used as a guide to target mRNAs containing either partially or fully complementary sequences, ultimately leading to down regulation of the corresponding proteins. It was previously shown that the kinase CK1α phosphorylates a cluster of residues in the eukaryotic insertion (EI) of Ago, leading to the alleviation of miRNA-mediated repression through an undetermined mechanism. We show that binding of miRNA-loaded human Ago2 to target RNA with complementarity to the seed and 3’ supplemental regions of the miRNA primes the EI for hierarchical phosphorylation by CK1α. The added negative charges electrostatically promote target release, freeing Ago to seek out additional targets once it is dephosphorylated. The high conservation of potential phosphosites in the EI suggests that such a regulatory strategy may be a shared mechanism for regulating miRNA-mediated repression.
Release of acidic store calcium is required for effective priming of the NLRP3 inflammasome
Authors: Platt Nick , Shepherd Dawn , Weng Yuzhe , Churchill Grant C. , Galione Antony , Platt Frances M. 
Published: January 2022

AbstractThe lysosome is a dynamic signaling organelle that is critical for cell functioning. It is a regulated calcium store that can contribute to Ca2+-regulated processes via both local calcium release and more globally by influencing ER Ca2+ release. Here, we provide evidence from studies of an authentic mouse model of the lysosomal storage disease Niemann-Pick Type C (NPC) that has reduced lysosomal Ca2+ levels, and genetically modified mice in which the two-pore lysosomal Ca2+ release channel family are deleted that lysosomal Ca2+ signaling is required for normal pro-inflammatory responses. We demonstrate that production of the pro-inflammatory cytokine IL-1β via the NLRP3 inflammasome is significantly reduced in murine Niemann-Pick Type C, the inhibition is selective because secretion of TNFα is not diminished and it is a consequence of inefficient inflammasome priming. Synthesis of precursor ProIL-1β is significantly reduced in macrophages genetically deficient in the lysosomal protein Npc1, which is mutated in most clinical cases of NPC, and in wild type cells in which Npc1 activity is pharmacologically inhibited. Comparable reductions in ProIL-1β generation were measured in vitro and in vivo by macrophages (MΦ) genetically altered to lack expression of the two-pore lysosomal Ca2+ release channels Tpcn1 or Tpcn2. These data demonstrate a requirement for lysosome-dependent Ca2+ signaling in the generation of specific pro-inflammatory responses.
Receptor interacting protein kinase-3 mediates both myopathy and cardiomyopathy in preclinical animal models of Duchenne muscular dystrophy
Authors: Bencze Maximilien , Periou Baptiste , Punzón Isabel , Barthélémy Inès , Taglietti Valentina , Hou Cyrielle , Zaidan Louai , Kefi Kaouthar , Blot Stéphane , Agbulut Onnik , Gervais Marianne , Derumeaux Geneviève , Tiret Laurent , Authier François-Jérôme , Relaix Fréderic 
Published: January 2022

AbstractBackgroundDuchenne muscular dystrophy (DMD) is a progressive muscle degenerative disorder, culminating in a complete loss of ambulation, hypertrophic cardiomyopathy and a fatal cardiorespiratory failure.Necroptosis is the form of necrosis that is dependent upon the receptor-interacting protein kinase (RIPK) 3; it is involved in several inflammatory and neurodegenerative conditions. We previously identified RIPK3 as a key player in the acute myonecrosis affecting the hindlimb muscles of the dystrophic mouse model, mdx. Whether necroptosis also mediates respiratory and heart disorders in DMD is currently unknown.MethodsEvidence of activation of the necroptotic axis was examined in dystrophic tissues from Golden retriever muscular dystrophy (GRMD) dogs and R-DMDdel52 rats. A functional assessment of the involvement of necroptosis in dystrophic animals was performed on mdx mice that were genetically depleted for RIPK3. Dystrophic mice aged from 12 to 18 months were analyzed by histology and molecular biology to compare the phenotype of muscles from mdxRipk3+/+and mdxRipk3-/-mice. Heart function was also examined by echocardiography in 40-week-old mice.ResultsQuantification ofRIPK3transcripts in sartorius and biceps femoris muscles from GRMD dogs positively correlated to myonecrosis levels (r=0.81; p=0.0076).RIPK3was also found elevated in the diaphragm (p=0<0.05). In the slow progressing heart phenotype of GRMD dogs, the phosphorylated form of RIPK1 at the Serine 161 site was dramatically increased in cardiomyocytes. A similar p-RIPK1 upregulation characterized the cardiomyocytes of R-DMDdel52 rats, associated with a marked overexpressionof Ripk1(p=0.007) andRipk3(p=0.008), indicating primed activation of the necroptotic pathway in the dystrophic heart. MdxRipk3-/-mice displayed decreased compensatory hypertrophy of the heart (p=0.014), and echocardiography showed a 19% increase in the relative wall thickness (p<0.05) and 29% reduction in the left ventricle mass (p=0.0144). Besides, mdxRipk3-/-mice presented no evidence of a regenerative default or sarcopenia in skeletal muscles, moreover around 50% less affected by fibrosis (p<0.05).ConclusionsOur data provide evidence of the activation of the necroptotic pathway in degenerative tissues from dystrophic animal models, including the diaphragm and the heart. The genetic inhibition of necroptosis in dystrophic mice improves both cardiac function and histological features of muscles, suggesting that prevention of necroptosis is susceptible to providing multiorgan beneficial effects for DMD.
Ligand bias underlies differential signaling of multiple FGFs via FGFR1
Authors: Karl Kelly , Del Piccolo Nuala , Light Taylor , Roy Tanaya , Dudeja Pooja , Ursachi Vlad-Constantin , Fafilek Bohumil , Krejci Pavel , Hristova Kalina 
Published: January 2022

AbstractThe mechanism of differential signaling of multiple FGF ligands through a single FGF receptor is poorly understood. Here, we use biophysical tools to quantify multiple aspects of FGFR1 signaling in response to FGF4, FGF8 and FGF9: potency, efficacy, bias, ligand-induced oligomerization and downregulation, and conformation of the active FGFR1 dimers. We find that the three ligands exhibit distinctly different potencies and efficacies for inducing responses in cells. We further discover qualitative differences in the actions of the three FGFs through FGFR1, as FGF8 preferentially activates some of the probed downstream responses (FRS2 phosphorylation and extracellular matrix loss), while FGF4 and FGF9 preferentially activate different probed responses (FGFR1 phosphorylation and cell growth arrest). Thus, FGF8 is a biased ligand, when compared to FGF4 and FGF9. Förster resonance energy transfer experiments reveal a correlation between biased signaling and the conformation of the FGFR1 transmembrane domain dimer. Our findings expand the mechanistic understanding of FGF signaling during development and bring the poorly understood concept of receptor tyrosine kinase ligand bias into the spotlight.