bluuebunny/crossref_metadata_2025 huggingface dataset:
Transcranial Magnetic stimulation (TMS) modulates functional activity of SH-SY5Y cells: An in vitro model provides support for assumed excitability changes
Authors: Thomson Alix C. , de Graaf Tom A. , Schuhmann Teresa , Kenis Gunter , Sack Alexander T. , Rutten Bart P.F.
Published: August 2020

Repetitive Transcranial Magnetic Stimulation (rTMS) is an established neuromodulation technique, using electromagnetic pulses that, depending on the precise parameters, are assumedto lead to lasting neural excitability changes. rTMS has widespread applications in both research and therapy, where it has been FDA approved and is considered a first-line treatment for depression, according to recent North American and European guidelines. However, these assumed excitability effects are often difficult to replicate, and highly unreliable on the single subject/patient level. Given the increasing application of rTMS, especially in clinical practice, the absence of a method to unequivocally determine effects of rTMS on human neuronal excitability is problematic. We have taken a first step in addressing this bottleneck, by administering excitatory and inhibitory rTMS protocols, iTBS and cTBS, to a humanin vitroneuron model; differentiated SH-SY5Y cells. We use live calcium imaging to assess changes in neural activity following stimulation, through quantifying fluorescence response to chemical depolarization. We found that iTBS and cTBS have opposite effects on fluorescence response; with iTBS increasing and cTBS decreasing response to chemical depolarization. Our results are promising, as they provide a clear demonstration of rTMS after-effects in a living human neuron model. We here present an in-vitro live calcium imaging setup that can be further applied to more complex human neuron models, for developing and evaluating subject/patient-specific brain stimulation protocols.
Gender (im)balance in citation practices in cognitive neuroscience
Authors: Fulvio Jacqueline M. , Akinnola Ileri , Postle Bradley R.
Published: August 2020

In the field of neuroscience, despite the fact that the proportion of peer-reviewed publications authored by women has increased in recent decades, the proportion of citations of women-led publications has not seen a commensurate increase: In five broad-scope journals, citations of papers first- and/or last-authored by women have been shown to be fewer than would be expected if gender was not a factor in citation decisions (Dworkin et al., 2020). Given the important implications that such underrepresentation may have on the careers of women researchers, it is important to determine whether this same trend is true in subdisciplines of the field, where interventions might be more effective. Here, we report the results of an extension of the analyses carried out by Dworkin et al. (2020) to citation patterns in the Journal of Cognitive Neuroscience (JoCN). The results indicate that the underrepresentation of women-led publications in reference sections is also characteristic of papers published inJoCNover the past decade. Furthermore, this pattern of citation imbalances is present for all gender classes of authors, implicating systemic factors. These results contribute to the growing body of evidence that intentional action is needed to address inequities in the way that we carry out and communicate our science.
Extreme Y chromosome polymorphism corresponds to five male reproductive morphs
Authors: Sandkam Benjamin A , Almeida Pedro , Darolti Iulia , Furman Benjamin , van der Bijl Wouter , Morris Jake , Bourne Godfrey , Breden Felix , Mank Judith E.
Published: August 2020

Sex chromosomes form once recombination is halted between the X and Y chromosomes. This loss of recombination quickly depletes Y chromosomes of functional content and genetic variation, which is thought to severely limit their potential to generate adaptive diversity. We examined Y diversity inPoecilia parae, where males occur as one of five discrete morphs, all of which shoal together in natural populations where morph frequency has been stable for over 50 years. Each morph utilizes different complex reproductive strategies, and differ dramatically from each other in color, body size, and mating behavior. Remarkably, morph phenotype is passed perfectly from father to son, indicating there are five Y haplotypes segregating in the species, each of which encodes the complex male morph characteristics. Using linked-read sequencing on multipleP. paraefemales and males of all five morphs from natural populations, we found that the genetic architecture of the male morphs evolved on the Y chromosome long after recombination suppression had occurred with the X. Comparing Y chromosomes between each of the morphs revealed that although the Ys of the three minor morphs that differ predominantly in color are highly similar, there are substantial amounts of unique genetic material and divergence between the Ys of the three major morphs that differ in reproductive strategy, body size and mating behavior. Taken together, our results reveal the extraordinary ability of evolution to overcome the constraints of recombination loss to generate extreme diversity resulting in five discrete Y chromosomes that control complex reproductive strategies.

Significance Statement

The loss of recombination on the Y chromosome is thought to limit the adaptive potential of this unique genomic region. Despite this, we describe an extraordinary case of Y chromosome adaptation inPoecilia parae. This species contains five co-occurring male morphs, all of which are Y-linked, and which differ in reproductive strategy, body size, coloration, and mating behavior. The five Y-linked male morphs ofP. paraeevolved after recombination was halted on the Y, resulting in five unique Y chromosomes within one species. Our results reveal the surprising magnitude to which non-recombining regions can generate adaptive diversity and have important implications for the evolution of sex chromosomes and the genetic control of sex-linked diversity.
Hemagglutination byB. fragilisis mediated by capsular polysaccharides and is influenced by host ABO blood type
Authors: Arnolds Kathleen L. , Moreno-Huizar Nancy , Stanislawski Maggie A. , Palmer Brent , Lozupone Catherine
Published: August 2020

Bacterial hemagglutination of red blood cells (RBCs) is mediated by interactions between bacterial cell components and RBC envelope glycans that vary across individuals by ABO blood type. ABO glycans are also expressed on intestinal epithelial cells and in most individuals secreted into the intestinal mucosa, indicating that hemagglutination by bacteria may be informative about bacteria-host interactions in the intestine.Bacteroides fragilis, a prominent member of the human gut microbiota, can hemagglutinate RBCs by an unknown mechanism. Using a novel technology for quantifying bacterial hemagglutination, genetic knockout strains ofB. fragilisand blocking antiserums, we demonstrate that the capsular polysaccharides ofB. fragilis, polysaccharide B (PSB), and PSC are both strong hemagglutinins. Furthermore, the capacity ofB. fragilisto hemagglutinate was much stronger in individuals with Type O blood compared to Types A and B, an adaptation that could impact the capacity ofB. fragilisto colonize and thrive in the host.

Importance Statement

This study found that the human pathobiont,B.fragilis, hemagglutinates human red blood cells using specific capsular polysaccharides (PSB and PSC) which are known to be important for interacting with and influencing host immune responses. Because the factors found on red blood cells are also abundantly expressed on other tissues and in the mucous, the ability to hemagglutinate sheds light on interactions between bacteria and host throughout the body. Intriguingly, the strength of hemagglutination varied based on the ABO blood type of the host, a finding which could have implications for understanding if an individual’s blood type may influence interactions withB.fragilisand its potential as a pathogen versus a commensal.
CD300lf conditional knockout mouse reveals strain-specific cellular tropism for murine norovirus
Authors: Graziano Vincent R. , Alfajaro Mia Madel , Schmitz Cameron O. , Filler Renata B. , Strine Madison S. , Wei Jin , Hsieh Leon L. , Baldridge Megan T. , Nice Timothy J. , Lee Sanghyun , Orchard Robert C. , Wilen Craig B.
Published: August 2020

Noroviruses are a leading cause of gastrointestinal infection in humans and mice. Understanding human norovirus (HuNoV) cell tropism has important implications for our understanding of viral pathogenesis. Murine norovirus (MNoV) is extensively used as a surrogate model for HuNoV. We previously identified CD300lf as the receptor for MNoV. Here, we generated aCd300lfconditional knockout (CD300lfF/F) mouse to elucidate the cell tropism of persistent and non-persistent strains of murine norovirus. Using this mouse model, we demonstrate that CD300lf expression on intestinal epithelial cells (IECs), and on tuft cells in particular, is essential for transmission of the persistent MNoV strain CR6 (MNoVCR6)in vivo. In contrast, the nonpersistent MNoV strain CW3 (MNoVCW3) does not require CD300lf expression on IECs for infection. However, deletion of CD300lf in myelomonocytic cells (LysM Cre+)partially reduces CW3 viral load in lymphoid and intestinal tissues. Disruption of CD300lf expression on B cells (CD19 Cre), neutrophils (Mrp8 Cre), and dendritic cells (CD11c Cre) did not affect CW3 viral RNA levels. Finally, we show that the transcription factor STAT1, which is critical for the innate immune response, partially restricts the cell tropism of MNoVCW3to LysM+ cells. Taken together, these data demonstrate that CD300lf expression on tuft cells is essential for MNoVCR6, that myelomonocytic cells are a major, but not exclusive, target cell of MNoVCW3, and that STAT1 signaling restricts the cellular tropism of MNoVCW3. This provides the first genetic system to study the cell type-specific role of CD300lf in norovirus pathogenesis.

IMPORTANCE

Human noroviruses (HuNoVs) are a leading cause of gastroenteritis resulting in up to 200,000 deaths each year. The receptor and cell tropism of HuNoV in immunocompetent humans are unclear. We use murine norovirus (MNoV) as a model for HuNoV. We recently identified CD300lf as the sole physiologic receptor for MNoV. Here, we leverage this finding to generate aCd300lfconditional knockout mouse to decipher the contributions of specific cell types to MNoV infection. We demonstrate that persistent MNoVCR6requires CD300lf expression on tuft cells. In contrast, multiple CD300lf+ cell types, dominated by myelomonocytic cells, are sufficient for non-persistent MNoVCW3infection. CD300lf expression on epithelial cells, B cells, neutrophils, and dendritic cells is not critical for MNoVCW3infection. Mortality associated with MNoVCW3strain inStat1-/-mice does not require CD300lf expression on LysM+ cells, highlighting that both CD300lf receptor expression and innate immunity regulate MNoV cell tropismin vivo.
Conformational ordering of intrinsically disordered peptides for targeting translation initiation
Authors: Brown Christopher J , Verma Chandra S , Lane David P , Lama Dilraj
Published: August 2020

Intrinsically disordered regions (IDRs) in proteins can regulate their activity by facilitating protein-protein interactions (PPIs) as exemplified in the recruitment of the eukaryotic translation initiation factor 4E (eIF4E) protein by the protein eIF4G. Deregulation of this PPI module is central to a broad spectrum of cancer related malignancies and its targeted inhibition through bioactive peptides is a promising strategy for therapeutic intervention. We have employed a structure-guided approach to rationally develop peptide derivatives from the intrinsically disordered eIF4G scaffold by incorporating non-natural amino acids that facilitates disorder-to-order transition. The conformational heterogeneity of these peptides and the degree of structural reorganization required to adopt the optimum mode of interaction with eIF4E underscores their differential binding affinities. The presence of a pre-structured local helical element in the ensemble of structures was instrumental in the efficient docking of the peptides on to the protein surface. These insights were exploited to further design features into the peptide to propagate bound-state conformations in solution which resulted in the generation of a potent eIF4E binder. The study illustrates the molecular basis of eIF4E recognition by a disordered epitope from eIF4G and its modulation to generate peptides that can potentially attenuate translation initiation in oncology.
Development of a high-throughput homogeneous AlphaLISA drug screening assay for the detection of SARS-CoV-2 Nucleocapsid
Authors: Gorshkov Kirill , Chen Catherine Z. , de la Torre Juan Carlos , Martinez-Sobrido Luis , Moran Thomas , Zheng Wei
Published: August 2020

The coronavirus disease 2019 (COVID-19) pandemic caused by Severe Acute Respiratory Syndrome coronavirus 2 (SARS-CoV-2) is in urgent need of therapeutic options. High-throughput screening (HTS) offers the research field an opportunity to rapidly identify such compounds. In this work, we have developed a homogeneous cell-based HTS system using AlphaLISA detection technology for the SARS-CoV-2 nucleocapsid protein (NP). Our assay measures both recombinant NP and endogenous NP from viral lysates and tissue culture supernatants (TCS) in a sandwich-based format using two monoclonal antibodies against the NP analyte. Viral NP was detected and quantified in both tissue culture supernatants and cell lysates, with large differences observed between 24 hours and 48 hours of infection. We simulated the viral infection by spiking in recombinant NP into 384-well plates with live Vero-E6 cells and were able to detect the NP with high sensitivity and a large dynamic range. Anti-viral agents that inhibit either viral cell entry or replication will decrease the AlphaLISA NP signal. Thus, this assay can be used for high-throughput screening of small molecules and biologics in the fight against the COVID-19 pandemic.
3D mapping reveals a complex and transient interstitial matrix during murine renal development
Authors: Lipp Sarah N. , Jacobson Kathryn R. , Hains David S. , Schwarderer Andrew L. , Calve Sarah
Published: August 2020

Background

The extracellular matrix (ECM) is a network of proteins and glycosaminoglycans that provides structural and biochemical cues to cells. In the kidney, the ECM is critical for nephrogenesis; however, the dynamics of ECM composition and how it relates to 3D structure during development is unknown.

Methods

Using embryonic day (E)14.5, E18.5, postnatal day (P)3, and adult kidneys, we fractionated proteins based on differential solubilities, performed liquid chromatography tandem-mass spectrometry, and identified changes in ECM protein content (matrisome). Decellularized kidneys were stained for ECM proteins and imaged in 3D using confocal microscopy.

Results

We observed an increase in interstitial ECM that connect the stromal mesenchyme to the basement membrane (TNXB, COL6A1, COL6A2, COL6A3) between the embryo and adult, and a transient elevation of interstitial matrix proteins (COL5A2, COL12A1, COL26A1, ELN, EMID1, FBN1, LTBP4, THSD4) at perinatal timepoints. Basement membrane proteins critical for metanephric induction (FRAS1, FREM2) were highest in the embryo, whereas proteins necessary for glomerular basement membrane integrity (COL4A3, COL4A4, COL4A5, LAMB2) were more abundant in the adult. 3D visualization revealed a complex interstitial matrix that dramatically changed over development, including the perinatal formation of fibrillar structures that appear to support the medullary rays.

Conclusion

By correlating 3D ECM spatiotemporal organization with global protein abundance, we identified novel changes in the interstitial matrix during kidney development. This new information regarding the ECM in developing kidneys offers the potential to inform the design of regenerative scaffolds that can guide nephrogenesisin vitro.

Significance statement

End-stage renal disease is increasing and there are a limited number of organs available for transplantation. Therefore, researchers have focused on understanding how cellular signaling influences kidney development to expand strategies to rebuild a kidney. However, the extracellular matrix (ECM), another critical component that biomechanically regulates nephrogenesis, has been largely neglected. This paper combines proteomics and 3D imaging of the murine kidney to resolve previously undescribed dynamics of the interstitial matrix in the cortex and corticomedullary junction during development. Combined with cell and growth factors, scaffolds modeled after the composition and organization of the developmental ECM have the potential to improve tissue engineering models of the kidney, like organoids.
Unravelling cytosolic delivery of endosomal escape peptides with a quantitative endosomal escape assay (SLEEQ)
Authors: Teo Serena L.Y. , Rennick Joshua J. , Yuen Daniel , Al-Wassiti Hareth , Johnston Angus P.R. , Pouton Colin W.
Published: August 2020

Endosomal escape is an essential requirement but a major obstacle to efficient delivery of therapeutic peptides, proteins and nucleic acids. Current understanding of endosomal escape mechanisms remains limited due to significant number of conflicting reports, which are compounded by low sensitivity and indirect assays. To resolve this, we developed a highly sensitive Split Luciferase Endosomal Escape Quantification (SLEEQ) assay to probe mechanisms of cytosolic delivery. We applied SLEEQ to evaluate the endosomal escape of a range of widely studied putative endosomal escape peptides (EEPs). We demonstrated that positively-charged EEPs enhanced cytosolic delivery as a result of increased non-specific cell membrane association, rather than increased endosomal escape efficiency. These findings transform our current understanding of how EEPs increase cytosolic delivery. SLEEQ is a powerful tool that addresses fundamental questions in intracellular drug delivery and will significantly improve the way materials are engineered to increase therapeutic delivery to the cytosol.
Identification of Chlorophyll a-b Binding Protein AB96 as a novel TGFβ1 binding agent
Authors: Lynham Steven , Freile Fabio Grundland , Puri Natasha M , O’Reilly Nicola , Mitchell Graham H , Wells Timothy N.C. , Willcox Merlin , Beatson Richard
Published: August 2020

The discovery of compounds and proteins from plants has greatly contributed to modern medicine, especially in malaria where both quinine and artemisinin have been the cornerstone of therapeutics. Here we describe the first known plant-derived cytokine binding agent. Chlorophyll a-b binding protein AB96, present to varying levels in the leaves of all chlorophyll-containing plants, binds to active TGFβ1. Active TGFβ1 contributes to the pathology of many infectious and neoplastic diseases and therefore, by inhibiting these processes, chlorophyll a-b binding protein opens up new approaches with therapeutic potential.
Neuronal death in pneumococcal meningitis is triggered by pneumolysin and pilus-1 interactions with β-actin
Authors: Tabusi Mahebali , Thorsdottir Sigrun , Lysandrou Maria , Narciso Ana Rita , Minoia Melania , Henriques-Normark Birgitta , Iovino Federico
Published: August 2020

Neuronal damage is a major consequence of bacterial meningitis, but little is known about mechanisms that lead to neuronal death.Streptococcus pneumoniae(pneumococcus) is a leading cause of bacterial meningitis and many survivors develop neurological sequelae after the acute infection has resolved, possibly due to neuronal damage. Here, we studied mechanisms for pneumococcal interactions with neurons. Using human primary neurons and co-immunoprecipitation assays, we showed that pneumococci interact with the cytoskeleton protein β-actin through the pilus-1 adhesin RrgA and the cytotoxin pneumolysin (Ply), thereby promoting adhesion and uptake into neurons and neuronal death. Using our bacteremia-derived meningitis mouse model, we observed that RrgA- and Ply-expressing pneumococci co-localize with neuronal β-actin. We found that pneumococcal-infected neurons show increased intracellular Ca2+ levels depending on RrgA and mainly Ply which likely cause actin cytoskeleton disassembly leading to neuronal damage. Finally, neuronal death caused by pneumococcal infection could be inhibited using antibody against β-actin.
Sulf2a controls Shh-dependent neural fate specification in the developing spinal cord
Authors: Danesin Cathy , Darche-Gabinaud Romain , Escalas Nathalie , Bouguetoch Vanessa , Cochard Philippe , Oustah Amir Al , Ohayon David , Glise Bruno , Soula Cathy
Published: August 2020

Sulf2a belongs to the Sulf family of extracellular sulfatases which selectively remove 6-O-sulfate groups from heparan sulfates, a critical regulation level for their role in modulating the activity of signalling molecules. Data presented here define Sulf2a as a novel player in the control of Sonic Hedgehog (Shh)-mediated cell type specification during spinal cord development. We show that Sulf2a depletion in zebrafish results in overproduction of V3 interneurons at the expense of motor neurons and also impedes generation of oligodendrocyte precursor cells (OPCs), three cell types that depend on Shh for their generation. We provide evidence that Sulf2a, expressed in a spatially restricted progenitor domain, acts by maintaining the correct patterning and specification of ventral progenitors. More specifically, Sulf2a prevents Olig2 progenitors to activate high-threshold Shh response and, thereby, to adopt a V3 interneuron fate, thus ensuring proper production of motor neurons and OPCs. We propose a model in which Sulf2a reduces Shh signalling levels in responding cells by decreasing their sensitivity to the morphogen factor. More generally, our work, revealing that, in contrast to its paralog Sulf1, Sulf2a regulates neural fate specification in Shh target cells, provides direct evidence of non-redundant functions of Sulfs in the developing spinal cord.
CK2 Phosphorylation is required for Regulation of Syntaxin 1A activity in Ca2+-triggered release in neuroendocrine cells
Authors: Barak-Broner Noa , Singer-Lahat Dafna , Chikvashvili Dodo , Lotan Ilana
Published: August 2020

The polybasic juxtamembrane region (5RK) of the plasma membrane neuronal SNARE, syntaxin1A (Syx), was shown by us to act as a fusion clamp in PC12 cells, making release dependent on stimulation by Ca2+. By using a Syx-based FRET probe, we demonstrated that 5RK is absolutely required for a depolarization-induced Ca+2-dependent, close-to-open transition (CDO) of Syx that involves the vesicular SNARE synaptobrevin2 and occurs concomitantly with Ca2+-triggered release. Here, we investigated the mechanism underlying the 5RK requirement, and identified phosphorylation of Syx at Ser-14 (S14) by protein kinase CK2 as a crucial molecular determinant. Following biochemical verification that both endogenous Syx and CSYS are constitutively S14 phosphorylated in PC12 cells, dynamic FRET analysis of phospho-null and phospho-mimetic mutants of CSYS and the use of a CK2 inhibitor revealed that it is the S14 phosphorylation that confers the 5RK requirement. Concomitant amperometric analysis of catecholamine release revealed that the phospho-null mutants do not support release, spontaneous and evoked. Collectively, these results identify a functionally important CK2 phosphorylation site in Syx that is required for 5RK-regulation of CDO and for concomitant Ca2+-triggered release.

Summary statement

Many phospho-proteins participate in vesicle exocytosis. We show that a recently identified structural transition of syntaxin1A that accompanies Ca2+-regulated exocytosis in neuroendocrine cells is controlled by CK2 phosphorylation of syntaxin1A.
Segmentation boosting with compensation methods in optical coherence tomography angiography images
Authors: Lee Yih-Cherng , Ding Jian-Jiun , Yeung Ling , Lee Tay-Wey , Chang Chia-Jung , Lin Yu-Tze , Chang Ronald Y.
Published: August 2020

Optical coherence tomography angiography is a noninvasive imaging modality to establish the diagnosis of retinal vascular diseases. However, angiography images are significantly interfered if patients jitter or blink. In this study, a novel retinal image analysis method to accurately detect blood vessels and compensate the effect of interference was proposed. We call this the patch U-Net compensation (PUC) system, which is based on the famous U-Net. Several techniques, including a better training mechanism, direction criteria, area criteria, gap criteria, and probability map criteria, have been proposed to improve its accuracy. Simulations show that the proposed PUC achieves much better performance than state-of-art methods.
Primary carbohydrate metabolism genes participate in heat stress memory at the shoot apical meristem ofArabidopsis thaliana
Authors: Olas Justyna Jadwiga , Apelt Federico , Annunziata Maria Grazia , Richard Sarah Isabel , Gupta Saurabh , Kragler Friedrich , Balazadeh Salma , Mueller-Roeber Bernd
Published: August 2020

Although we have a good understanding of the development of shoot apical meristems (SAM) in higher plants, and the function of the stem cells (SCs) embedded in the SAM, there is surprisingly little known of its molecular responses to abiotic stresses. Here, we show that the SAM ofArabidopsis thalianasenses heat stress (HS) and retains an autonomous molecular memory of a previous non-lethal HS, allowing the SAM to regain growth after exposure to an otherwise lethal HS several days later. Using RNA-seq, we identified genes participating in establishing a SAM-specific HS memory. The genes includeHEAT SHOCK TRANSCRIPTION FACTORs(HSFs), of whichHSFA2is essential, but not sufficient, for full HS memory in the SAM, the SC regulatorsCLAVATA1(CLV1) andCLV3, and several primary carbohydrate metabolism genes, includingFRUCTOSE-BISPHOSPHATE ALDOLASE 6(FBA6). We found that expression ofFBA6during HS at the SAM complements that ofFBA8in the same organ. Furthermore, we show that sugar availability at the SAM is essential for survival at high-temperature HS. Collectively, plants have evolved a sophisticated protection mechanism to maintain SCs and, hence, their capacity to re-initiate shoot growth after stress release.
Genetic evidence indicates new distribution record of endangered Kashmir musk deer (Moschus cupreus) with range expansion in Uttarakhand, India
Authors: Kumar Ajit , Singh Bhim , Sahoo Subhashree , Gautam Kumudani Bala , Gupta Sandeep Kumar
Published: August 2020

Kashmir musk deer, KMD (Moschus cupreus) is one the most threatened species reported from the Himalayan region of Kashmir, Pakistan and Afghanistan. A comprehensive and reliable distribution range of musk deer is still lacking. Recently, a molecular study confirmed the presence of KMD in Mustang in Nepal, west of Annapurna Himalayas. Here, we investigated the phylogenetic relationship of musk deer from Jammu and Kashmir (J&K), Kedarnath Wildlife Sanctuary (KWLS), and Nanda Devi Biosphere Reserve (NDBR), Uttarakhand region, India based on mitochondrial control region. The Bayesian phylogenetic analysis indicated a close genetic relationship between samples from J&K, KWLS and NDBR with identified lineages of KMD from Nepal with high posterior probabilities (PP∼100). It confirmed that the musk deer lineage from the Uttarakhand region of KWLS (1025-3662 m) and NDBR (1800-7817 m) to be of KMD (M. cupreus) and hence a distinct Evolutionary Significant Unit (ESU). Besides, as per the IUCN database, the Western Himalayan region also holds the population ofM. leucogasterandM. chrysogaster. Hence, we suggest extensive sampling for proper identification and validation of the geographic limits of musk deer species. We report for the first time the existence of KMD from the Uttarakhand region that we recommend to be updated in the IUCN database. It will assist in the effective conservation and management of this enigmatic endangered species.
Context-dependent behavioral plasticity compromises disruptive selection on sperm traits in squid
Authors: Hirohashi Noritaka , Sato Noriyosi , Iwata Yoko , Tomano Satoshi , Alam Md Nur E , Escolar Oscar , Fernández-Álvarez Fernando Ángel , Villanueva Roger , Apostólico Lígia Haselmann , Marian José Eduardo Amoroso Rodriguez
Published: August 2020

Male animals are not given equal mating opportunities under competitive circumstances. Small males often exhibit alternative mating behaviours and produce spermatozoa of higher quality to compensate for their lower chances of winning physical contests against larger competitors [1]. Because the reproductive benefits of these phenotypes depend on social status/agonistic ranks that can change during growth or aging [2], sperm traits should be developed/switched into fitness optima according to their prospects. However, reproductive success largely relies upon social contexts arising instantaneously from intra- and inter-sexual interactions, which deter males from developing extreme traits and instead favour behavioural plasticity. Nevertheless, the extent to which such plasticity influences developmentally regulated alternative sperm traits remains unexplored. Squids of the family Loliginidae are excellent models to investigate this, because they show sophisticated alternative reproductive tactics (ARTs) by which small males, known as “sneakers”, produce longer spermatozoa and perform extra-pair copulation to attach their sperm packages near the female seminal receptacle (SR). In contrast, large “consort” males have shorter spermatozoa and copulate via pair-bonding to insert their sperm packages near the internal female oviduct [3]. In addition, plasticity in male mating behaviour is common in some species while it is either rare or absent in others. Thus, squid ARTs display a broad spectrum of adaptive traits with a complex repertoire in behaviour, morphology and physiology [3].
Specialized terminology limits the reach of new scientific knowledge
Authors: Martínez Alejandro , Mammola Stefano
Published: August 2020

Words are the building blocks of science. As our understanding of the world progresses, scientific disciplines naturally enrich their specialized vocabulary (jargon). However, in the era of interdisciplinarity, the use of jargon may hinder effective communication amongst scientists that do not share a common linguistic background. The question of how jargon limits the transmission of scientific knowledge has long been debated, but rarely addressed quantitatively. We explored the relationship between the use of jargon and citations using 21,486 articles focusing on cave research, a multidisciplinary field particularly prone to terminological specialization and where linguistic disagreement among peers is frequent. We demonstrate that the use of jargon in the title and abstract significantly reduces the number of citations a paper receives. Given that these elements are the hook to readers, we urge scientists to restrict jargon to sections of the paper where its use is unavoidable.
Effects of fine-scale population structure on the distribution of heterozygosity in a long-term study ofAntirrhinum majus
Authors: Surendranadh Parvathy , Arathoon Louise , Baskett Carina A. , Field David L. , Pickup Melinda , Barton Nicholas H.
Published: August 2020

Many studies have quantified the distribution of heterozygosity and relatedness in natural populations, but surprisingly few have examined the demographic processes driving these patterns. In this study we take a novel approach by studying how population structure affects both pairwise identity and the distribution of heterozygosity in a natural population of a self-incompatible plantAntirrhinum majus. We look at a measure of the variance in heterozygosity within a population, identity disequilibrium (g2), together with FSTusing a panel of 91 SNPs in 22,353 individuals collected over 11 years. We find that pairwise relatedness (FST) declines rapidly over short spatial scales, and the excess variance in heterozygosity between individuals (g2) reflects significant variation in inbreeding. Additionally, we detect an excess of individuals with around half the average heterozygosity, indicating that some are due to selfing or matings between close relatives. We use two types of simulation to ask whether variation in heterozygosity is consistent with fine-scale spatial population structure. First, by simulating offspring using parents drawn from a range of spatial scales, we show that the known pollen dispersal kernel explainsg2. Second, we simulate a 1000-generation pedigree using the known dispersal and spatial distribution and find that the resultingg2is consistent with that observed from the field data. In contrast, a simulated population with uniform density underestimatesg2, indicating that heterogeneous density promotes identity disequilibrium. Our study shows that heterogeneous density and leptokurtic dispersal can together explain the distribution of heterozygosity. Furthermore, our study highlights the limitations of making theoretical predictions from simulations that only assume simple density and dispersal distributions.
Patterning the embryonic pulmonary mesenchyme
Authors: Goodwin Katharine , Jaslove Jacob M. , Tao Hirotaka , Zhu Min , Hopyan Sevan , Nelson Celeste M.
Published: August 2020

Smooth muscle guides morphogenesis of several epithelia during organogenesis, including the mammalian airways. However, it remains unclear how airway smooth muscle differentiation is spatiotemporally patterned and whether it originates from distinct mesenchymal progenitors. Using single-cell RNA-sequencing of embryonic mouse lungs, we show that the pulmonary mesenchyme contains a continuum of cell identities, but no distinct progenitors. Transcriptional variability correlates with sub-epithelial and sub-mesothelial mesenchymal compartments that are regulated by Wnt signaling. Live-imaging and tension-sensors reveal compartment-specific migratory behaviors and cortical forces, and show that sub-epithelial mesenchyme contributes to airway smooth muscle. Cytoskeletal and Wnt signaling pathways are activated early in reconstructed differentiation trajectories. Consistently, Wnt activation stimulates the earliest stages of smooth muscle differentiation and induces local accumulation of mesenchymal F-actin, which influences epithelial morphology. Our single-cell approach uncovers the principles of pulmonary mesenchymal patterning during branching morphogenesis and identifies a morphogenetically active mesenchymal layer that sculpts the airway epithelium.
Defining the RBPome of T helper cells to study higher order post-transcriptional gene regulation
Authors: Hoefig Kai P. , Reim Alexander , Gallus Christian , Wong Elaine H. , Behrens Gesine , Conrad Christine , Xu Meng , Ito-Kureha Taku , Defourny Kyra , Geerlof Arie , Mautner Josef , Hauck Stefanie M. , Baumjohann Dirk , Feederle Regina , Mann Matthias , Wierer Michael , Glasmacher Elke , Heissmeyer Vigo
Published: August 2020

Post-transcriptional gene regulation is complex, dynamic and ensures proper T cell function. The targeted transcripts can simultaneously respond to various factors as evident forIcos, an mRNA regulated by several RNA binding proteins (RBPs), including Roquin. However, fundamental information about the entire RBPome involved in post-transcriptional gene regulation in T cells is lacking. Here, we applied global RNA interactome capture (RNA-IC) and orthogonal organic phase separation (OOPS) to human and mouse primary T cells and identified the core T cell RBPome. This defined 798 mouse and 801 human proteins as RBPs, unexpectedly containing signaling proteins like Stat1, Stat4 and Vav1. Based on the vicinity to Roquin-1 in proximity labeling experiments, we selected ∼50 RBPs for testing coregulation of Roquin targets. Induced expression of these candidate RBPs in wildtype and Roquin-deficient T cells unraveled several Roquin-independent contributions, but also revealed Celf1 as a new Roquin-1-dependent and target-specific coregulator ofIcos.

One sentence statement

We provide an atlas of RNA-binding proteins in human and mouse T helper cells as a resource for studying higher order post-transcriptional gene regulation.
Dynamics of transcriptional programs and chromatin accessibility in mouse spermatogonial cells from early postnatal to adult life
Authors: Lazar-Contes Irina , Arzate-Mejia Rodrigo G. , Tanwar Deepak K. , Steg Leonard C. , Uzel Kerem , Feudjio Olivier Ulrich , Crespo Marion , Germain Pierre-Luc , Mansuy Isabelle M.
Published: August 2020

In mammals, spermatogonial cells (SPGs) are undifferentiated male germ cells in testis that are quiescent until birth and then self-renew and differentiate to produce spermatogenic cells and functional sperm from early postnatal life throughout adulthood. The transcriptome of SPGs is highly dynamic and timely regulated during postnatal development. We examined if such dynamics involves changes in chromatin organization by profiling the transcriptome and chromatin accessibility of SPGs from early postnatal stages to adulthood in mice using deep RNA-seq, ATAC-seq and computational deconvolution analyses. By integrating transcriptomic and epigenomic features, we show that SPGs undergo massive chromatin remodeling during postnatal development that partially correlates with distinct gene expression profiles and transcription factors (TF) motif enrichment. We identify genomic regions with significantly different chromatin accessibility in adult SPGs that are marked by histone modifications associated with enhancers and promoters. Some of the regions with increased accessibility correspond to transposable element subtypes enriched in multiple TFs motifs and close to differentially expressed genes. Our results underscore the dynamics of chromatin organization in developing germ cells and complement existing datasets on SPGs by providing maps of the regulatory genome at high resolution from the same cell populations at early postnatal, late postnatal and adult stages collected from single individuals.
An evolutionary model identifies the main selective pressures for the evolution of genome-replication profiles
Authors: Droghetti Rossana , Agier Nicolas , Fischer Gilles , Gherardi Marco , Lagomarsino Marco Cosentino
Published: August 2020

Recent results comparing the temporal program of genome replication of yeast species belonging to theLachanceaclade support the scenario that the evolution of replication timing program could be mainly driven by correlated acquisition and loss events of active replication origins. Using these results as a benchmark, we develop an evolutionary model defined as birth-death process for replication origins, and use it to identify the selective pressures that shape the replication timing profiles. Comparing different evolutionary models with data, we find that replication origin birth and death events are mainly driven by two evolutionary pressures, the first imposes that events leading to higher double-stall probability of replication forks are penalized, while the second makes less efficient origins more prone to evolutionary loss. This analysis provides an empirically grounded predictive framework for quantitative evolutionary studies of the replication timing program.
Colony expansions underlie the evolution of army ant mass raiding
Authors: Chandra Vikram , Gal Asaf , Kronauer Daniel J. C.
Published: August 2020

Collective behavior emerges from local interactions between group members, and natural selection can fine-tune these interactions to achieve different collective outcomes. However, at least in principle, collective behavior can also evolve via changes in group-level parameters. Here, we show that army ant mass raiding, an iconic collective behavior in which many thousands of ants spontaneously leave the nest to go hunting, has evolved from group raiding, in which a scout directs a much smaller group of ants to a specific target. We describe the structure of group raids in the clonal raider ant, a close relative of army ants. We find that the coarse structure of group raids and mass raids is highly conserved, and that army ants and their relatives likely follow similar behavioral rules, despite the fact that their raids differ strikingly in overall appearance. By experimentally increasing colony size in the clonal raider ant, we show that mass raiding gradually emerges from group raiding without altering individual behavioral rules. This suggests a simple mechanism for the evolution of army ant mass raids, and more generally that scaling effects may provide an alternative mechanism for evolutionary transitions in complex collective behavior.
Soft X-ray induced radiation damage in thin freeze-dried brain samples studied by FTIR microscopy
Authors: Surowka Artur D. , Gianoncelli A. , Birarda G. , Sala S. , Cefarin N. , Matruglio A. , Szczerbowska-Boruchowska M. , Ziomber-Lisiak A. , Vaccari L.
Published: August 2020

In order to push the spatial resolution limits to the nanoscale, synchrotron-based soft X-ray microscopy (XRM) experiments require higher radiation doses to be delivered to materials. Nevertheless, the associated radiation damage impacts on the integrity of delicate biological samples. Herein, the extent of soft X-ray radiation damage in popular thin freeze-dried brain tissue samples mounted onto Si3N4 membranes, as highlighted by Fourier transform infrared microscopy (FTIR), is reported. The freeze-dried tissue samples were found to be affected by general degradation of the vibrational architecture, though these effects were weaker than those observed in paraffin-embedded and hydrated systems reported in the literature. In addition, weak, reversible and specific features of the tissue–Si3N4 interaction could be identified for the first time upon routine soft X-ray exposures, further highlighting the complex interplay between the biological sample, its preparation protocol and X-ray probe.
Combining valproate and bipyridyl ligands to construct a 0D core-shell Zn5(μ3-OH)2 cluster and a 2D layered coordination network with a [Zn3(μ3-OH)]2 SBU
Authors: Abu Ali Hijazi , Darawsheh Mohanad
Published: August 2020

Starting from the proposed zinc carboxylate cluster tetrakis(μ-2-propylpentanoato)dizinc(II), Zn2(μ2-valp)4 (I), of valproic acid, a branched short-chain fatty acid, and bipyridine ligands, two new mixed-ligand coordination compounds, namely, bis(2,2′-bipyridine)di-μ3-hydroxido-hexakis(μ-2-propylpentanoato)bis(2-propylpentanoato)pentazinc(II), [Zn5(C8H15O2)8(OH)2(C10H8N2)2] (II), and poly[[bis(μ-4,4′-bipyridine)di-μ3-hydroxido-octakis(μ-2-propylpentanoato)bis(2-propylpentanoato)hexazinc(II)] dimethylformamide disolvate], {[Zn6(C8H15O2)10(OH)2(C10H8N2)2]·2C3H7NO}
n
(III), were synthesized. Compound II is a core-shell-type zero-dimensional discrete Zn5(μ3-OH)2 metal–organic cluster with Zn ions in double-triangle arrangements that share one Zn ion coincident with an inversion centre. The cluster contains three crystallographically non-equivalent Zn ions exhibiting three different coordination geometries (tetrahedral, square pyramidal and octahedral). The cluster cores are well separated and embedded in a protective shell of the aliphatic branched short chains of valproate. As a result, there is no specific interaction between the discrete clusters. Conversely, compound III, a 2D layered coordination network with a secondary building unit (SBU), is formed by Zn6(μ3-OH)2 clusters exhibiting a chair-like hexagonal arrangement. This SBU is formed from two Zn3(μ3-OH) trimers related by inversion symmetry and connected by two syn–anti bridging carboxylate groups. Each SBU is connected by four 4,4′-bipyridine ligands producing a 63-hcb net topology. 2D coordination layers are sandwiched within layers of dimethylformamide molecules that do not interact strongly with the network due to the hydrophobic protection provided by the valproate ligands.
Tilings by hexagonal prisms and embeddings into primitive cubic networks
Authors: Bouniaev Mikhail M. , Dolbilin Nikolay P. , Shtogrin Mikhail I.
Published: August 2020

All possible combinatorial embeddings into primitive cubic networks of arbitrary tilings of 3D space by pairwise congruent and parallel regular hexagonal prisms are discussed and classified.
TlPO3and its comparison with isotypic RbPO3and CsPO3
Authors: Weil Matthias
Published: August 2020

The crystal structure of thallium(I)catena-polyphosphate, TlPO3, contains a polyphosphate chain extending parallel to [010] with a repeating unit of two phosphate tetrahedra. The TlIatom is located in-between the polyphosphate chains and is bonded by oxygen atoms in a distorted [6 + 1] coordination in the form of a monocapped prism, with the longest Tl—O bond to the bridging O atom of the polyphosphate chain. A quantitative structural comparison with isotypic RbPO3and CsPO3reveals that the usually pronounced stereoactivity of the 6s2lone pair at the TlIatom is not apparent in the case of TlPO3.
Annual reporting by social enterprise organizations: “legitimacy surplus” or reporting deficit?
Authors: Connolly Ciaran , Kelly Martin
Published: August 2020

Purpose

Drawing on an accountability framework developed for social enterprise organizations (SEOs), this paper examines the annual report disclosure practices of SEOs in the United Kingdom in order to investigate the types of accountability disclosed by SEOs.

Design/methodology/approach

After developing a SEO database, and utilizing a bespoke document coding checklist, the annual reports of 129 SEOs were examined.

Findings

The results indicate that while SEOs would be expected to account in line with normative stakeholder theory, many do not provide constructive and voluntary accountability information to their stakeholders, at least through the annual report, and that their focus is on satisfying legal obligations.

Originality/value

In response to calls for research to better understand accountability in new organizational contexts, this paper makes two contributions: firstly, by extending prior accountability research in the NFP sector to consider organizational hybrids, it raises questions about organizational accountability and how it is discharged in situations where an organization operates as a business and yet is accountable for its social mission; secondly, assuming these organizations are driven by their business and social logics, the findings suggest that SEO accountability disclosure practices are inconsistent with the social objectives on which they are based.