bluuebunny/crossref_metadata_2025_split huggingface dataset:
Unveiling how herpetofauna cope with land-use changes— insights from forest-cashew-rice landscapes in West Africa
Authors: dos Reis-Silva Francisco , Pizzigalli Cristian , Seck Sambu , Cabeza Mar , Rainho Ana , Rocha Ricardo , Palmeirim Ana Filipa 
Published: June 2024

AbstractAgricultural-induced land-use change comprises a key driver of biodiversity loss across tropical forests. Guinea-Bissau, in West Africa, was formerly occupied by native forest-savanna mosaics. While savannas have long gave place to traditional rice agroecosystems, forests are now being transformed into cashew monocultures at unprecedented rates. The ecological impact of such rapid change is largely unknown. Here, we examined how rarefied species richness, abundance, and composition of amphibians and reptiles varied across forest remnants, cashew orchards and rice paddies in northern Guinea-Bissau. To do so, visual encounter surveys were carried across 21 sampling sites, seven in each habitat type. A total of 703 amphibian and 266 reptile encounters was recorded from nine and 14 taxa, respectively. The results show class-specific responses to habitat type. Amphibian diversity in forest remnants and cashew orchards remained similar, but rice paddies harboured higher abundance and distinct composition compared to forest remnants. Reptile abundance was highest in cashew orchards, which comprised a distinct species composition, when compared to forest remnants. Rice paddies sustained lower reptile richness and abundance. Overall, our results do not support the expected detrimental impacts of cashew expansion, which might be due to the still high heterogeneity of habitat types within the landscape. Rice paddies proved particularly important for amphibians, and for open-habitat reptiles, boosting the landscape-scale species diversity. In face of the eminent habitat conversion, maintaining heterogeneous landscapes, including the persistence of both forest remnants and rice paddies, is critical to minimize biodiversity loss in West Africa.
Structural basis of dual BACH1 regulation by SCFFBXO22and SCFFBXL17
Authors: Goretzki Benedikt , Khoshouei Maryam , Penner Patrick , Stephan Christine , Argoti Dayana , Dierlamm Nele , Rada Jimena Maria , Kapps Sandra , Thiel Zacharias , Mutlu Merve , Furkert David , Müller Catrin Swantje , Freuler Felix , Haenni Simon , Tenaillon Laurent , Knapp Britta , Hinniger Alexandra , Hoppe Philipp , Gutmann Sascha , Ryzhakov Grigory , Schmidt Enrico , Iurlaro Mario , Fernández César 
Published: June 2024

SummaryBTB and CNC homolog 1 (BACH1) is a master transcriptional regulator of the cellular oxidative stress response and pro-metastatic oncogene. Post-translational stability of BACH1 is tightly regulated by distinct F-box ubiquitin ligases, including SCFFBXO22and SCFFBXL17. However, the molecular details have been elusive. Here, we reveal a structural switch in FBXO22 that controls the recognition of a three-dimensional degron in the BACH1 BTB domain, thus explaining its specificity for dimeric BACH1. We describe how cancer-associated mutations in FBXO22 modulate binding and ubiquitylation of BACH1. Further, we reveal that cancer-related mutations or cysteine-modifications destabilize the BTB domain and redirect BACH1 to FBXL17, where it is recognized as a monomer. This explains how complementary ligases post-translationally regulate BACH1 depending on the state of its BTB domain. Our findings provide mechanistic insights into the regulation of the oxidative stress response and may spur therapeutic strategies to targeting oxidative stress-related disorders and metastatic cancers.
Defective interferon signaling in the circulating monocytes of type 2 diabetic mice
Authors: Omodaka Shunsuke , Kato Yuya , Sato Yoshimichi , Falcone-Juengert Jaime , Zhang Hongxia , Kanoke Atsushi , Eckalbar Walter L. , Endo Hidenori , Hsieh Christine L. , Aran Dvir , Liu Jialing 
Published: June 2024

AbstractType 2 diabetes mellitus (T2DM) is associated with poor outcome after stroke. Peripheral monocytes play a critical role in the secondary injury and recovery of damaged brain tissue after stroke, but the underlying mechanisms are largely unclear. To investigate transcriptome changes and molecular networks across monocyte subsets in response to T2DM and stroke, we performed single-cell RNA-sequencing (scRNAseq) from peripheral blood mononuclear cells and bulk RNA-sequencing from blood monocytes from four groups of adult mice, consisting of T2DM modeldb/dband normoglycemic controldb/+mice with or without ischemic stroke. Via scRNAseq we found that T2DM expands the monocyte population at the expense of lymphocytes, which was validated by flow cytometry. Among the monocytes, T2DM also disproportionally increased the inflammatory subsets with Ly6C+ and negative MHC class II expression (MO.6C+II−). Conversely, monocytes from control mice without stroke are enriched with steady-state classical monocyte subset of MO.6C+II+ but with the least percentage of MO.6C+II− subtype. Apart from enhancing inflammation and coagulation, enrichment analysis from both scRNAseq and bulk RNAseq revealed that T2DM specifically suppressed type-1 and type-2 interferon signaling pathways crucial for antigen presentation and the induction of ischemia tolerance. Preconditioning by lipopolysaccharide conferred neuroprotection against ischemic brain injury indb/+but not indb/dbmice and coincided with a lesser induction of brain Interferon-regulatory-factor-3 in the brains of the latter mice. Our results suggest that the increased diversity and altered transcriptome in the monocytes of T2DM mice underlie the worse stroke outcome by exacerbating secondary injury and potentiating stroke-induced immunosuppression.Significance StatementThe mechanisms involved in the detrimental diabetic effect on stroke are largely unclear. We show here, for the first time, that peripheral monocytes have disproportionally altered the subsets and changed transcriptome under diabetes and/or stroke conditions. Moreover, genes in the IFN-related signaling pathways are suppressed in the diabetic monocytes, which underscores the immunosuppression and impaired ischemic tolerance under the T2DM condition. Our data raise a possibility that malfunctioned monocytes may systemically and focally affect the host, leading to the poor outcome of diabetes in the setting of stroke. The results yield important clues to molecular mechanisms involved in the detrimental diabetic effect on stroke outcome.
OsAAI1-OsMADS25 module orchestrates root morphogenesis by fine-tuning IAA in drought stressed rice
Authors: Xu Ning , Luo Rui , Long Qing , Man Jianmin , Yin Jiaxi , Liao Haimin , Jiang Meng 
Published: June 2024

AbstractIndole-3-acetic acid (IAA) plays a critical role as a plant hormone in regulating the growth and development of the root system in plants, particularly in enhancing their ability to withstand abiotic stress. In this study, we found that overexpression ofOsAAI1promoted the growth of rice root system. The length of primary root, the number of lateral roots, the density of lateral roots, and the number of adventitious roots of overexpression ofOsAAI1(OE19) were significantly better than those of the wild type (ZH11) and the mutant line (osaai1), and the IAA content of OE19 was significantly higher than those of ZH11 andosaai1. We also found that exogenous application of IAA could compensate for the root growth defect caused by theosaai1mutation. OE19 had the highest number and widest distribution of total roots under the water-cut drought treatment, and exogenous application of IAA attenuated the growth inhibitory effect of drought stress onosaai1. Our study also revealed that OsAAI1 interacts with the MADS-box family transcription factor OsMASD25. Additionally, the application of IAA helped alleviate the growth inhibitory effects of drought stress onosmads25.Importantly, OsMADS25 interaction with OsAAI1 was found to enhance the transcriptional expression of its downstream target genesLAX1andOsBAG4, which are crucial genes in rice’s response to drought stress. These findings suggest that OsAAI1 and OsMADS25 are crucial in rice’s drought acclimation process by regulating downstream gene expression and influencing the IAA signaling pathway.Author summaryThe root system is a crucial organ for crop plants as it facilitates the absorption of water and nutrients, contributing to their drought resistance. Indole-3-acetic acid (IAA) plays a pivotal role in the growth of various types of roots in plants. Under drought stress conditions, changes in IAA levels and transport can impact the morphology of plant roots. This research illustrates that OsAAI1 positively influences rice root development and enhances the plant’s response to drought stress through the auxin signaling pathway. The study reveals a physical interaction between OsAAI1 and the transcription factor OsMADS25. This interaction boosts the expression of the auxin synthesis geneOsYUC4and suppresses the auxin inhibitory factorOsIAA14, thereby promoting the auxin signaling pathway, stimulating rice root growth, and enhancing the plant’s ability to withstand drought. Furthermore, the interaction between OsAAI1 and OsMADS25 has been found to also positively affect the expression of the genesLAX1andOsBAG4, which is associated with activated drought resistance in rice plants.
Post-flowering photoperiod sensitivity of soybean in pod-setting responses
Authors: Sun Zhihui , Yuan LiMei , Wang Yulin , Fang Ran , Lin Xiaoya , Li Haiyang , Chen Liyu , Wu Yichun , Huang Xin , Kong Fanjiang , Liu Baohui , Lu Sijia , Kong Lingping 
Published: June 2024

AbstractThe development of soybean (Glycine max) is regulated by photoperiod, with genes related to photoperiod sensitivity primarily focused on flowering time. However, their roles in post-flowering reproductive development and the mechanisms by which photoperiod affects them are not yet determined. In this study, we found that pod formation is sensitive to photoperiod. Long-day (LD) conditions tend to extend the time from flowering to pod formation (R1 to R3 stage), and the first wave of flowers tends to fall off. Additionally, photoperiod affects pistil morphology; under short-day (SD) conditions, the stigma has a curved hook-like structure that facilitates better interaction with the filaments when pollen is released, ultimately influencing the timing of pod formation. Photoperiod-insensitive mutants, lackingE1family andEvening Complexgenes, showed no difference in pod formation time under LD or SD conditions. Hormone content analysis and transcriptome data analysis indicated that various hormones, ROS signals, and the application of sucrose solutionin vitromight influence floral organ abscission.HighlightPhotoperiod sensitivity after flowering affects the pod-setting time in soybean.
Direct prediction of intermolecular interactions driven by disordered regions
Authors: Ginell Garrett M. , Emenecker Ryan. J , Lotthammer Jeffrey M. , Usher Emery T. , Holehouse Alex S. 
Published: June 2024

ABSTRACTIntrinsically disordered regions (IDRs) are critical for a wide variety of cellular functions, many of which involve interactions with partner proteins. Molecular recognition is typically considered through the lens of sequence-specific binding events. However, a growing body of work has shown that IDRs often interact with partners in a manner that does not depend on the precise order of the amino acid order, instead driven by complementary chemical interactions leading to disordered bound-state complexes. Despite this emerging paradigm, we lack tools to describe, quantify, predict, and interpret these types of structurally heterogeneous interactions from the underlying amino acid sequences. Here, we repurpose the chemical physics developed originally for molecular simulations to develop an approach for predicting intermolecular interactions between IDRs and partner proteins. Our approach enables the direct prediction of phase diagrams, the identification of chemically-specific interaction hotspots on IDRs, and a route to develop and test mechanistic hypotheses regarding IDR function in the context of molecular recognition. We use our approach to examine a range of systems and questions to highlight its versatility and applicability.
HAdV-5 infection dysregulates cysteine, purine, and unsaturated fatty acid metabolism in fibroblasts
Authors: Sanchez Bailey-J C. , Ortiz Rudy M. , Grasis Juris A. 
Published: June 2024

AbstractViral infections can cause cellular dysregulation of metabolic reactions. Viruses alter host metabolism to meet their replication needs. The impact of viruses on specific metabolic pathways is not well understood, even for a well-studied virus-like human adenovirus. Adenoviral infection is known to affect cellular glycolysis and respiration, however, global effects on cellular metabolic pathways in response to adenoviral infection are lacking, particularly in normally quiescent structural cells, such as fibroblasts. Further, few studies have employed an untargeted approach with an emphasis on viral dosage and duration of infection. To address this, we employed untargeted metabolomics to quantify the dynamic metabolic shifts in fibroblasts infected with human adenovirus serotype 5 (HAdV-5) at three dosages (0.5, 1.0, and 2.0 multiplicity of infection [MOI]) and across four time points (6, 12, 24, and 36 h post-infection [HPI]). The greatest differences in individual metabolites were observed at 6– and 12-hours post-infection. In addition to its effects on glycolysis and respiration, adenoviral infection downregulated cysteine and unsaturated fatty acid metabolism, while upregulated purine metabolism. These results reveal the specific metabolic pathways that are perturbed by adenoviral infection and the associated dynamic shifts in metabolism, suggesting that viral infections alter energetics via profound changes in protein, lipid, and nucleic acid metabolism. The results revealed previously unconsidered metabolic pathways disrupted by HAdV-5 that can alter cells, even in non-excitable structural cells, such as fibroblasts.ImportanceHuman adenoviruses overtake the DNA replication machinery of the infected host, rewiring mitotic events and leading to effects on cellular respiration and glycolysis. Fibroblast lineages are normally quiescent cells that display a repertoire of responses to certain agonists. While metabolism often begins with glucose breakdown in the form of aerobic glycolysis, additional pathways are important for the overall functioning of the cell. Data on shifts in the metabolism of fibroblast cells in response to human adenoviral infection are lacking. We used an untargeted metabolomic approach to better understand the dynamic metabolic changes in human kidney cells in response to three viral dosages across four time points post infection. Profound shifts were observed for the cysteine, purine, and unsaturated fatty acid metabolites. This analysis provides a global perspective and highlights previously underappreciated aspects of how human adenoviruses alter host metabolism.
Discovery of Novel Long Non-Coding RNAs with potential role in zebrafish brain regeneration
Authors: Kohli Surbhi , Abhilash Dasari , Hemlata  , Srivastava Priyanka P. , Kumar Vishantan , Minocha Shilpi , Gupta Ishaan 
Published: June 2024

AbstractUnderstanding brain regeneration mechanisms is vital for treating neurological conditions. Zebrafish (Danio rerio) are an excellent model due to their genetic similarity to humans and strong regenerative abilities. In this study, we identified novel long non-coding RNAs (lncRNAs) in the regenerating zebrafish brain following traumatic brain injury (TBI). RNA sequencing data of the zebrafish telencephalon from the BioStudies database was analyzed for novel long non-coding RNA expression (lncRNA) at control, one day post-lesion (early wound healing), three days post-lesion (cell proliferation), and 14 days post-lesion (differentiation). We identified 689 potential lncRNAs using HISAT2, StringTie, FEELnc, and PhastCon analysis tools. Principal component analysis (PCA) of identified lncRNAs revealed a distinct expression profile at 1-day post-lesion, indicating their significant role in early wound healing.Weighted Gene Co-expression Network Analysis (WGCNA) identified two modules (brown and turquoise) showing unique expression patterns critical to brain regeneration. Pathway enrichment analysis linked brown module lncRNAs to peptide biosynthesis, cellular amide metabolism, and ribosome biogenesis. In contrast, turquoise module lncRNAs were associated with ion transmembrane transport and cell adhesion pathways. qPCR validation confirmed co-expression patterns of selected lncRNAs and correlated genes, emphasizing their regulatory roles. This study demonstrates that lncRNAs play crucial roles in zebrafish brain regeneration by modulating gene expression during the early wound healing stage. These insights offer potential therapeutic applications of lncRNAs in neuroregenerative medicine.
Cognitive behavioral phenotyping ofDSCAMheterozygosity as a model for autism spectrum disorder
Authors: Neff Ryan C. , Stangis Katherine A. , Beniwal Ujjawal , Hergenreder Ty , Ye Bing , Murphy Geoffrey G. 
Published: June 2024

AbstractIt is estimated that 1 in 36 children are affected by autism spectrum disorder (ASD) in the United States, which is nearly a twofold increase from a decade ago. Recent genetic studies have identifiedde novoloss-of-function (dnLoF) mutations in theDown Syndrome Cell Adhesion Molecule (DSCAM)as a strong risk factor for ASD. Previous research has shown thatDSCAMablation confers social interaction deficits and perseverative behaviors in mouse models. However, it remains unknown to what extentDSCAMunderexpression captures the full range of behaviors, specifically cognitive phenotypes, presented in ASD. Here, we conducted a comprehensive cognitive behavioral phenotyping which revealed that loss of one copy ofDSCAM, as in theDSCAM2J+/− mice, displayed hyperactivity, increased anxiety, and motor coordination impairments. Additionally, hippocampal-dependent learning and memory was affected, including working memory, long-term memory, and contextual fear learning. Interestingly, implicit learning processes remained intact. Therefore,DSCAMLoF produces autistic-like behaviors that are similar to human cases of ASD. These findings further support a role forDSCAMdnLoF mutations in ASD and suggestDSCAM2J+/− as a suitable model for ASD research.Summary StatementAutism spectrum disorder represents a growing patient population. Loss of one copy of theDSCAMgene provides a promising mouse model that reproduces autistic-like behaviors for research and therapeutic testing.
Mechanism of how the universal module XMAP215 γ-TuRC nucleates microtubules
Authors: McManus Collin T. , Travis Sophie M. , Jeffrey Philip D. , Zhang Rui , Petry Sabine 
Published: June 2024

ABSTRACTIt has become increasingly evident in recent years that nucleation of microtubules from a diverse set of MTOCs requires both the γ-tubulin ring complex (γ-TuRC) and the microtubule polymerase XMAP215. Despite their essentiality, little is known about how these nucleation factors interact and work together to generate microtubules. Using biochemical domain analysis of XMAP215 and structural approaches, we find that a sixth TOG domain in XMAP215 binds γ-TuRCviaγ-tubulin as part of a broader interaction involving the C-terminal region. Moreover, TOG6 is required for XMAP215 to promote nucleation from γ-TuRC to its full extent. Interestingly, we find that XMAP215 also depends strongly on TOG5 for microtubule lattice binding and nucleation. Accordingly, we report a cryo-EM structure of TOG5 bound to the microtubule lattice that reveals promotion of lateral interactions between tubulin dimers. Finally, we find that while XMAP215 constructs’ effects on nucleation are generally proportional to their effects on polymerization, formation of a direct complex with γ-TuRC allows cooperative nucleation activity. Thus, we propose that XMAP215’s C-terminal TOGs 5 and 6 play key roles in promoting nucleation by promoting formation of longitudinal and lateral bonds in γ-TuRC templated nascent microtubules at cellular MTOCs.
Integration of Biological Data via NMF for Identification of Human Disease-Associated Gene Modules through Multi-label Classification
Authors: Alberuni Syed , Ray Sumanta 
Published: June 2024

AbstractExtensive evidence recognizes that proteins associated with several diseases frequently interact with each other. This leads to develop different network-based methods for uncovering the molecular workings of human diseases. These methods are based on the idea that protein interaction networks act as maps, where diseases manifest as localized perturbations within a neighborhood. Identifying these areas, known as disease modules, is essential for in-depth research into specific disease characteristics. While many computational methods have been developed the underlying connectivity patterns within these modules still yet to be explored. This work aim to fill this gap by integrating multiple biological data sources through non-negative matrix factorization (NMF) technique. We leverage two biological sources of information, protein-protein interactions (PPIs) and Gene Ontology data to find connections between novel genes and diseases. The data sources are first converted into networks, which are then clustered to obtain modules. Two types of modules are then integrated through NMF-based technique to obtain a set of meta-modules which preserve the essential characteristics of interaction patterns and functional similarity information among the proteins/genes. We assign multiple labels to each meta-module based on the statistical and biological properties they shared with the disease dataset. A multi-label classification technique is utilized to assign new disease labels to genes within each meta-modules. A total of 3131 gene-disease associations are identified, which are also validated through a literature survey, gene ontology and pathway-based analysis.
Perturbative computations of neutron-proton scattering observables using renormalization-group invariant chiral effective field theory up to
N3LO
Authors: Thim Oliver , Ekström Andreas , Forssén Christian 
Published: June 2024

We predict neutron-proton scattering cross sections and polarization observables up to next-to-next-to-next-to-leading order in a renormalization-group invariant description of the strong nucleon-nucleon interaction. Low-energy constants are calibrated to phase shifts, subleading corrections are computed in distorted-wave perturbation theory, and we employ momentum-cutoff values 500 and 2500 MeV. We find a steady order-by-order convergence and realistic descriptions of scattering observables up to a laboratory scattering energy of approximately 100 MeV. We also compare perturbative and nonperturbative calculations for phase shifts and cross sections and quantify how unitarity is gradually restored at higher orders. The perturbative approach offers an important diagnostic tool for any power counting and our results suggest that the breakdown scale in chiral effective field theory might be significantly lower than estimates obtained in nonperturbative calculations.

Published by the American Physical Society
2024