bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification and cultivation of anaerobic bacterial scavengers of dead cells
Authors: Hirakata Yuga , Mei Ran , Morinaga Kana , Katayama Taiki , Tamaki Hideyuki , Meng Xian-ying , Watari Takahiro , Yamaguchi Takashi , Hatamoto Masashi , Nobu Masaru K 
Published: October 2023

Abstract
The cycle of life and death and Earth’s carbon cycle(s) are intimately linked, yet how bacterial cells, one of the largest pools of biomass on Earth, are recycled back into the carbon cycle remains enigmatic. In particular, no bacteria capable of scavenging dead cells in oxygen-depleted environments have been reported thus far. In this study, we discover the first anaerobes that scavenge dead cells and the two isolated strains use distinct strategies. Based on live-cell imaging, transmission electron microscopy, and hydrolytic enzyme assays, one strain (designated CYCD) relied on cell-to-cell contact and cell invagination for degrading dead food bacteria where as the other strain (MGCD) degraded dead food bacteria via excretion of lytic extracellular enzymes. Both strains could degrade dead cells of differing taxonomy (bacteria and archaea) and differing extents of cell damage, including those without artificially inflicted physical damage. In addition, both depended on symbiotic metabolic interactions for maximizing cell degradation, representing the first cultured syntrophic Bacteroidota. We collectively revealed multiple symbiotic bacterial decomposition routes of dead prokaryotic cells, providing novel insight into the last step of the carbon cycle.
Chromatin-modifying enzymes as modulators of nuclear size during lineage differentiation
Authors: Meng Lingjun 
Published: October 2023

AbstractThe mechanism of nuclear size determination and alteration during normal lineage development and cancer pathologies which is not fully understood. As recently reported, chromatin modification can change nuclear morphology. Therefore, we screened a range of pharmacological chemical compounds that impact the activity of chromatin-modifying enzymes, in order to get a clue of the specific types of chromatin-modifying enzymes that remarkably effect nuclear size and shape. We found that interrupted activity of chromatin-modifying enzymes is associated with nuclear shape abnormalities. Furthermore, the activity of chromatin-modifying enzymes perturbs cell fate determination in cellular maintenance and lineage commitment. Our results indicated that chromatin-modifying enzyme regulates cell fate decision during lineage differentiation and is associate with nuclear size alteration.
Domain adapted brain network fusion captures variance related to pubertal brain development and mental health
Authors: Kraft Dominik , Alnæs Dag , Kaufmann Tobias 
Published: October 2023

AbstractPuberty demarks a period of profound brain dynamics that orchestrates changes to a multitude of neuroimaging-derived phenotypes. This complexity poses a dimensionality problem when attempting to chart an individual’s brain development over time. Here, we illustrate that shifts in subject similarity of brain imaging data relate to pubertal maturation in the longitudinal ABCD study. Given that puberty depicts a critical window for emerging mental health issues, we additionally show that our model is capable of capturing variance in the adolescent brain related to psychopathology in a population-based and a clinical cohort. These results suggest that low-dimensional reference spaces based on subject similarities render useful to chart variance in brain development in youths.
A deep population reference panel of tandem repeat variation
Authors: Ziaei Jam Helyaneh , Li Yang , DeVito Ross , Mousavi Nima , Ma Nichole , Lujumba Ibra , Adam Yagoub , Maksimov Mikhail , Huang Bonnie , Dolzhenko Egor , Qiu Yunjiang , Kakembo Fredrick Elishama , Joseph Habi , Onyido Blessing , Adeyemi Jumoke , Bakhtiari Mehrdad , Park Jonghun , Javadzadeh Sara , Jjingo Daudi , Adebiyi Ezekiel , Bafna Vineet , Gymrek Melissa 
Published: October 2023

AbstractTandem repeats (TRs) represent one of the largest sources of genetic variation in humans and are implicated in a range of phenotypes. Here we present a deep characterization of TR variation based on high coverage whole genome sequencing from 3550 diverse individuals from the 1000 Genomes Project and H3Africa cohorts. We develop a method, EnsembleTR, to integrate genotypes from four separate methods resulting in high-quality genotypes at more than 1.7 million TR loci. Our catalog reveals novel sequence features influencing TR heterozygosity, identifies population-specific trinucleotide expansions, and finds hundreds of novel eQTL signals. Finally, we generate a phased haplotype panel which can be used to impute most TRs from nearby single nucleotide polymorphisms (SNPs) with high accuracy. Overall, the TR genotypes and reference haplotype panel generated here will serve as valuable resources for future genome-wide and population-wide studies of TRs and their role in human phenotypes.
A non-canonical striatopallidal Go pathway that supports motor control
Authors: Labouesse Marie A. , Torres-Herraez Arturo , Chohan Muhammad O. , Villarin Joseph M. , Greenwald Julia , Sun Xiaoxiao , Zahran Mysarah , Tang Alice , Lam Sherry , Veenstra-VanderWeele Jeremy , Lacefield Clay O. , Bonaventura Jordi , Michaelides Michael , Chan C. Savio , Yizhar Ofer , Kellendonk Christoph 
Published: October 2023

AbstractIn the classical model of the basal ganglia, direct pathway striatal projection neurons (dSPNs) send projections to the substantia nigra (SNr) and entopeduncular nucleus to regulate motor function. Recent studies have re-established that dSPNs also possess axon collaterals within the globus pallidus (GPe) (bridging collaterals), yet the significance of these collaterals for behavior is unknown. Here we use in vivo optical and chemogenetic tools combined with deep learning approaches in mice to dissect the roles of dSPN GPe collaterals in motor function. We find that dSPNs projecting to the SNr send synchronous motor-related information to the GPe via axon collaterals. Inhibition of native activity in dSPN GPe terminals impairs motor activity and function via regulation of Npas1 neurons. We propose a model by which dSPN GPe axon collaterals (striatopallidal Go pathway) act in concert with the canonical terminals in the SNr to support motor control by inhibiting Npas1 neurons.
A reprogrammable mechanical metamaterial with origami functional-group transformation and ring reconfiguration
Authors: Hu Xinyu , Tan Ting , Wang Benlong , Yan Zhimiao 
Published: October 2023

AbstractRecent advancements in reprogrammable metamaterials have enabled the development of intelligent matters with variable special properties in situ. These metamaterials employ intra-element physical reconfiguration and inter-element structural transformation. However, existing mono-characteristic homo-element mechanical metamaterials have limited reprogramming functions. Here, we introduce a reprogrammable mechanical metamaterial composed of origami elements with heterogeneous mechanical properties, which achieves various mechanical behavior patterns by functional group transformations and ring reconfigurations. Through the anisotropic assembly of two heterogeneous elements into a functional group, we enable mechanical behavior switching between positive and negative stiffness. The resulting polygonal ring exhibits rotational deformation, zero Poisson’s ratio stretching/compression deformation, and negative Poisson’s ratio auxetic deformation. Arranging these rings periodically yields homogeneous metamaterials. The reconfiguration of quadrilateral rings allows for continuous fine-tunability of the mechanical response and negative Poisson’s ratio. This mechanical metamaterial could provide a versatile material platform for reprogrammable mechanical computing, multi-purpose robots, transformable vehicles and architectures at different scales.
The liver microenvironment orchestrates FGL1-mediated immune escape and progression of metastatic colorectal cancer
Authors: Li Jia-Jun , Wang Jin-Hong , Tian Tian , Liu Jia , Zheng Yong-Qiang , Mo Hai-Yu , Sheng Hui , Chen Yan-Xing , Wu Qi-Nian , Han Yi , Liao Kun , Pan Yi-Qian , Zeng Zhao-Lei , Liu Ze-Xian , Yang Wei , Xu Rui-Hua , Ju Huai-Qiang 
Published: October 2023

AbstractColorectal cancer (CRC) patients with liver metastases usually obtain less benefit from immunotherapy, and the underlying mechanisms remain understudied. Here, we identify that fibrinogen-like protein 1 (FGL1), secreted from cancer cells and hepatocytes, facilitates the progression of CRC in an intraportal injection model by reducing the infiltration of T cells. Mechanistically, tumor-associated macrophages (TAMs) activate NF-ĸB by secreting TNFα/IL-1β in the liver microenvironment and transcriptionally upregulate OTU deubiquitinase 1 (OTUD1) expression, which enhances FGL1 stability via deubiquitination. Disrupting the TAM-OTUD1-FGL1 axis inhibits metastatic tumor progression and synergizes with immune checkpoint blockade (ICB) therapy. Clinically, high plasma FGL1 levels predict poor outcomes and reduced ICB therapy benefits. Benzethonium chloride, an FDA-approved antiseptics, curbs FGL1 secretion, thereby inhibiting liver metastatic tumor growth. Overall, this study uncovers the critical roles and posttranslational regulatory mechanism of FGL1 in promoting metastatic tumor progression, highlighting the TAM-OTUD1-FGL1 axis as a potential target for cancer immunotherapy.
Synapsin condensation controls synaptic vesicle sequestering and dynamics
Authors: Hoffmann Christian , Rentsch Jakob , Tsunoyama Taka A. , Chhabra Akshita , Aguilar Perez Gerard , Chowdhury Rajdeep , Trnka Franziska , Korobeinikov Aleksandr A. , Shaib Ali H. , Ganzella Marcelo , Giannone Gregory , Rizzoli Silvio O. , Kusumi Akihiro , Ewers Helge , Milovanovic Dragomir 
Published: October 2023

AbstractNeuronal transmission relies on the regulated secretion of neurotransmitters, which are packed in synaptic vesicles (SVs). Hundreds of SVs accumulate at synaptic boutons. Despite being held together, SVs are highly mobile, so that they can be recruited to the plasma membrane for their rapid release during neuronal activity. However, how such confinement of SVs corroborates with their motility remains unclear. To bridge this gap, we employ ultrafast single-molecule tracking (SMT) in the reconstituted system of native SVs and in living neurons. SVs and synapsin 1, the most highly abundant synaptic protein, form condensates with liquid-like properties. In these condensates, synapsin 1 movement is slowed in both at short (i.e., 60-nm) and long (i.e., several hundred-nm) ranges, suggesting that the SV-synapsin 1 interaction raises the overall packing of the condensate. Furthermore, two-color SMT and super-resolution imaging in living axons demonstrate that synapsin 1 drives the accumulation of SVs in boutons. Even the short intrinsically-disordered fragment of synapsin 1 was sufficient to restore the native SV motility pattern in synapsin triple knock-out animals. Thus, synapsin 1 condensation is sufficient to guarantee reliable confinement and motility of SVs, allowing for the formation of mesoscale domains of SVs at synapses in vivo.
How myosin VI traps its off-state, is activated and dimerizes
Authors: Canon Louise , Kikuti Carlos , Planelles-Herrero Vicente J. , Lin Tianming , Mayeux Franck , Sirkia Helena , Lee Young il , Heidsieck Leila , Velikovsky Léonid , David Amandine , Liu Xiaoyan , Moussaoui Dihia , Forest Emma , Höök Peter , Petersen Karl J. , Morgan Tomos E. , Di Cicco Aurélie , Sirés-Campos Julia , Derivery Emmanuel , Lévy Daniel , Delevoye Cédric , Sweeney H. Lee , Houdusse Anne 
Published: October 2023

AbstractMyosin VI (Myo6) is the only minus-end directed nanomotor on actin, allowing it to uniquely contribute to numerous cellular functions. As for other nanomotors, the proper functioning of Myo6 relies on precise spatiotemporal control of motor activity via a poorly defined off-state and interactions with partners. Our structural, functional, and cellular studies reveal key features of myosin regulation and indicate that not all partners can activate Myo6. TOM1 and Dab2 cannot bind the off-state, while GIPC1 binds Myo6, releases its auto-inhibition and triggers proximal dimerization. Myo6 partners thus differentially recruit Myo6. We solved a crystal structure of the proximal dimerization domain, and show that its disruption compromises endocytosis in HeLa cells, emphasizing the importance of Myo6 dimerization. Finally, we show that the L926Q deafness mutation disrupts Myo6 auto-inhibition and indirectly impairs proximal dimerization. Our study thus demonstrates the importance of partners in the control of Myo6 auto-inhibition, localization, and activation.
Lipocalin 2 regulates mitochondrial phospholipidome remodeling, dynamics, and function in brown adipose tissue in male mice
Authors: Su Hongming , Guo Hong , Qiu Xiaoxue , Lin Te-Yueh , Qin Chao , Celio Gail , Yong Peter , Senders Mark , Han Xianlin , Bernlohr David A. , Chen Xiaoli 
Published: October 2023

AbstractMitochondrial function is vital for energy metabolism in thermogenic adipocytes. Impaired mitochondrial bioenergetics in brown adipocytes are linked to disrupted thermogenesis and energy balance in obesity and aging. Phospholipid cardiolipin (CL) and phosphatidic acid (PA) jointly regulate mitochondrial membrane architecture and dynamics, with mitochondria-associated endoplasmic reticulum membranes (MAMs) serving as the platform for phospholipid biosynthesis and metabolism. However, little is known about the regulators of MAM phospholipid metabolism and their connection to mitochondrial function. We discover that LCN2 is a PA binding protein recruited to the MAM during inflammation and metabolic stimulation. Lcn2 deficiency disrupts mitochondrial fusion-fission balance and alters the acyl-chain composition of mitochondrial phospholipids in brown adipose tissue (BAT) of male mice. Lcn2 KO male mice exhibit an increase in the levels of CLs containing long-chain polyunsaturated fatty acids (LC-PUFA), a decrease in CLs containing monounsaturated fatty acids, resulting in mitochondrial dysfunction. This dysfunction triggers compensatory activation of peroxisomal function and the biosynthesis of LC-PUFA-containing plasmalogens in BAT. Additionally, Lcn2 deficiency alters PA production, correlating with changes in PA-regulated phospholipid-metabolizing enzymes and the mTOR signaling pathway. In conclusion, LCN2 plays a critical role in the acyl-chain remodeling of phospholipids and mitochondrial bioenergetics by regulating PA production and its function in activating signaling pathways.
UV-induced G4 DNA structures recruit ZRF1 which prevents UV-induced senescence
Authors: De Magis Alessio , Limmer Michaela , Mudiyam Venkat , Monchaud David , Juranek Stefan , Paeschke Katrin 
Published: October 2023

AbstractSenescence has two roles in oncology: it is known as a potent tumor-suppressive mechanism, which also supports tissue regeneration and repair, it is also known to contribute to reduced patient resilience, which might lead to cancer recurrence and resistance after therapy. Senescence can be activated in a DNA damage-dependent and -independent manner. It is not clear which type of genomic lesions induces senescence, but it is known that UV irradiation can activate cellular senescence in photoaged skin. Proteins that support the repair of DNA damage are linked to senescence but how they contribute to senescence after UV irradiation is still unknown. Here, we unraveled a mechanism showing that upon UV irradiation multiple G-quadruplex (G4) DNA structures accumulate in cell nuclei, which leads to the recruitment of ZRF1 to these G4 sites. ZRF1 binding to G4s ensures genome stability. The absence of ZRF1 triggers an accumulation of G4 structures, improper UV lesion repair, and entry into senescence. On the molecular level loss of ZRF1 as well as high G4 levels lead to the upregulation of DDB2, a protein associated with the UV-damage repair pathway, which drives cells into senescence.
Pathogen-driven degradation of endogenous and therapeutic antibodies during streptococcal infections
Authors: Toledo Alejandro Gomez , Bratanis Eleni , Velásquez Erika , Chowdhury Sounak , Olofsson Berit , Sorrentino James T. , Karlsson Christofer , Lewis Nathan E. , Esko Jeffrey D. , Collin Mattias , Shannon Oonagh , Malmström Johan 
Published: October 2023

AbstractGroup A streptococcus (GAS) is a major bacterial pathogen responsible for both local and systemic infections in humans. The molecular mechanisms that contribute to disease heterogeneity remain poorly understood. Here we show that the transition from a local to a systemic GAS infection is paralleled by pathogen-driven alterations in IgG homeostasis. Using animal models and a combination of sensitive proteomics and glycoproteomics readouts, we documented the progressive accumulation of IgG cleavage products in plasma, due to extensive enzymatic degradation triggered by GAS infection in vivo. The level of IgG degradation was modulated by the route of pathogen inoculation, and mechanistically linked to the combined activities of the bacterial protease IdeS and the endoglycosidase EndoS, upregulated during infection. Importantly, we show that these virulence factors can alter the structure and function of exogenous therapeutic IgG in vivo. These results shed light on the role of bacterial virulence factors in shaping GAS pathogenesis, and potentially blunting the efficacy of antimicrobial therapies.
Switchable photothermal conversion efficiency for reprogrammable actuation
Authors: He Yongcheng , Liu Haojun , Luo Jiajia , Li Nuo , Li Lihua , Xiong Puxian , Gan Jiulin , Yang Zhongmin 
Published: October 2023

AbstractReprogrammable soft matter brings flexibility to soft robots so that they can display various motions, which is flourishing in soft robotics. However, the reprogramming of photoresponsive materials used in soft robots is time-consuming using existing methods. In this study, we promote a strategy for rapid reprogramming via switchable photothermal conversion efficiency (PCE). The liquid crystalline elastomers doped with semiconductor bismuth compounds (Bi-LCE) used in this work exhibited large photothermal actuation with over 35% shrinkage in 5 s at high PCE state, which demonstrated little deformation at low PCE state. Furthermore, the material was capable of being reprogrammed up to 10 times, with only 20 min required for one PCE reversible switch. Based on this switchable PCE effect, the same Bi-LCE film displayed various shape changes through different programmable pattern. Additionally, a reprogrammable hollow tube made of PCE reprogrammable materials could tune the diameter, cross-section configuration, and surface morphology, which was crucial for microfluidics field. Reprogrammable materials provide endless possibilities for reusability and sustainability in robotics.
Detection of the infrared aurora at Uranus with Keck-NIRSPEC
Authors: Thomas Emma M. , Melin Henrik , Stallard Tom S. , Chowdhury Mohammad N. , Wang Ruoyan , Knowles Katie , Miller Steve 
Published: October 2023

AbstractNear-infrared (NIR)-wavelength observations of Uranus have been unable to locate any infrared aurorae, despite many attempts to do so since the 1990s. While at Jupiter and Saturn, NIR investigations have redefined our understanding of magnetosphere–ionosphere–thermosphere coupling, the lack of NIR auroral detection at Uranus means that we have lacked a window through which to study these processes at Uranus. Here we present NIR Uranian observations with the Keck II telescope taken on the 5 September 2006 and detect enhanced H3+ emissions. Analysing temperatures and column densities, we identify an 88% increase in localized H3+ column density, with no significant temperature increases, consistent with auroral activity generating increased ionization. By comparing these structures against the Q3mp magnetic-field model and the Voyager 2 ultraviolet observations, we suggest that these regions make up sections of the northern aurora.
Mechanical disengagement of the cohesin ring
Authors: Richeldi Martina , Pobegalov Georgii , Higashi Torahiko L. , Gmurczyk Karolina , Uhlmann Frank , Molodtsov Maxim I. 
Published: October 2023

AbstractCohesin forms a proteinaceous ring that is thought to link sister chromatids by entrapping DNA and counteracting the forces generated by the mitotic spindle. Whether individual cohesins encircle both sister DNAs and how cohesin opposes spindle-generated forces remains unknown. Here we perform force measurements on individual yeast cohesin complexes either bound to DNA or holding together two DNAs. By covalently closing the hinge and Smc3Psm3–kleisin interfaces we find that the mechanical stability of the cohesin ring entrapping DNA is determined by the hinge domain. Forces of ~20 pN disengage cohesin at the hinge and release DNA, indicating that ~40 cohesin molecules are sufficient to counteract known spindle forces. Our findings provide a mechanical framework for understanding how cohesin interacts with sister chromatids and opposes the spindle-generated tension during mitosis, with implications for other force-generating chromosomal processes including transcription and DNA replication.
Chronic dehydration induces injury pathways in rats, but does not mimic histopathology of chronic interstitial nephritis in agricultural communities
Authors: Schreurs Gerd , Maudsley Stuart , Nast Cynthia , Praet Marleen , Da Silva Fernandes Sylvina , Boor Peter , D’Haese Patrick , De Broe Marc E. , Vervaet Benjamin A. 
Published: October 2023

AbstractCINAC-patients present renal proximal tubular cell lysosomal lesions which are also observed in patients experiencing calcineurin inhibitor (CNI) nephrotoxicity, suggesting that CINAC is a toxin-induced nephropathy. An alternative hypothesis advocates chronic dehydration as a major etiological factor for CINAC. Here, we evaluated histological and molecular changes in dehydrated versus toxin exposed rats. Wistar rats were divided in 3 groups. Group 1 (n = 6) had free access to drinking water (control group). Group 2 (n = 8) was water deprived for 10 h per 24 h, 5 days/week and placed in an incubator (37 °C) for 30 min/h during water deprivation. Group 3 (n = 8) underwent daily oral gavage with cyclosporine (40 mg/kg body weight). After 28 days, renal function, histopathology and proteomic signatures were analysed. Cyclosporine-treated rats developed focal regions of atrophic proximal tubules with associated tubulo-interstitial fibrosis. PASM staining revealed enlarged argyrophilic granules in affected proximal tubules, identified as lysosomes by immunofluorescent staining. Electron microscopy confirmed the enlarged and dysmorphic phenotype of the lysosomes. Overall, these kidney lesions resemble those that have been previously documented in farmers with CINAC. Dehydration resulted in none of the above histopathological features. Proteomic analysis revealed that dehydration and cyclosporine both induce injury pathways, yet of a clear distinct nature with a signature of toxicity only for the cyclosporine group. In conclusion, both cyclosporine and dehydration are injurious to the kidney. However, dehydration alone does not result in kidney histopathology as observed in CINAC patients, whereas cyclosporine administration does. The histopathological analogy between CINAC and calcineurin inhibitor nephrotoxicity in rats and humans supports the involvement of an as-yet-unidentified environmental toxin in CINAC etiology.