Biology subjects

Liu, Y.

Publications and source records attributed to Liu, Y..

At least 1,153 records · Page 64Linked to original sources

bioRxiv2024

Acarbose ameliorates Western diet-induced metabolic and cognitive impairments in the 3xTg mouse model of Alzheimer's disease

Age is the greatest risk factor for Alzheimers disease (AD) as well as for other disorders that increase the risk of AD such as diabetes and obesity. There is growing interest in determining if interventions that promote metabolic health can prevent or delay AD. Acarbose is an anti-diabetic drug that not only improves glucose homeostasis, but also extends the lifespan of wild-type mice. Here, we test the hypothesis that acarbose will not only preserve metabolic health, but also slow or prevent AD pathology and cognitive deficits in 3xTg mice, a model of AD, fed either a Control diet or a high-fat, high-sucrose Western diet (WD). We find that acarbose decreases the body weight and adiposity of WD-fed 3xTg mice, increasing energy expenditure while also stimulating food consumption, and improves glycemic control. Both male and female WD-fed 3xTg mice have worsened cognitive deficits than Control-fed mice, and these deficits are ameliorated by acarbose treatment. Molecular and histological analysis of tau and amyloid pathology identified sex-specific effects of acarbose which are uncoupled from the dramatic improvements in cognition, suggesting that the benefits of acarbose on AD are largely driven by improved metabolic health. In conclusion, our results suggest that acarbose may be a promising intervention to prevent, delay, or even treat AD, especially in individuals consuming a Western diet.

physiology↗

bioRxiv2024

Cellular and Molecular Changes During Aging in MEC: Unveiling the Role of Bglap3 Neurons in Cognitive Aging

Aging-correlated cognitive declines, including deficiencies in spatial orientation and memory, may reflect dysfunction in the hippocampus and medial entorhinal cortex (MEC). However, aging-related changes in MEC at the cellular and molecular levels remain unclear. In this study, we found fewer grid cells with reduced spatial stability in old mice. We compared gene expression profiles between young and old mice using 10x Genomics Visium technology. Among 1664 differentially expressed genes, we discovered Bglap3, a marker gene for subpopulation in MEC Layer III with decreased cell number with age. Silencing of Bglap3+ neurons in young mice impaired the spatial tuning of neurons in MEC and the spatial learning of a new platform location in water maze. These findings help us to understand the cellular and molecular changes in the MEC in healthy aging animals and the changes of Bglap3+ cells in old mice indicating a possible cause of aging-related MEC deficiency.

neuroscience↗

bioRxiv2024

Collagen modification remodels the sarcoma tumor microenvironment and promotes resistance to immune checkpoint inhibition

Molecular mechanisms underlying immune checkpoint inhibitor (ICI) response heterogeneity in solid tumors, including soft tissue sarcomas (STS), remain poorly understood. Herein, we demonstrate that the collagen-modifying enzyme, procollagen-lysine,2-oxoglutarate 5-dioxygenase 2 (Plod2), which is over-expressed in many tumors relative to normal tissues, promotes immune evasion in undifferentiated pleomorphic sarcoma (UPS), a relatively common and aggressive STS subtype. This finding is consistent with our earlier observation that Plod2 promotes tumor metastasis in UPS, and its enzymatic target, collagen type VI (ColVI), enhances CD8+ T cell dysfunction. We determined that genetic and pharmacologic inhibition of Plod2 with the pan-Plod transcriptional inhibitor minoxidil, reduces UPS growth in an immune competent syngeneic transplant system and enhances the efficacy of anti-Pd1 therapy. These findings suggest that PLOD2 is an actionable cancer target and its modulation could augment immunotherapy responses in patients with UPS, and potentially other sarcomas and carcinomas.

cancer biology↗

bioRxiv2024

Structure-Mechanics Principles and Mechanobiology of Fibrocartilage Pericellular Matrix: A Pivotal Role of Type V Collagen

The pericellular matrix (PCM) is the immediate microniche surrounding resident cells in various tissue types, regulating matrix turnover, cell-matrix cross-talk and disease initiation. This study elucidated the structure-mechanical properties and mechanobiological functions of the PCM in fibrocartilage, a family of connective tissues that sustain complex tensile and compressive loads in vivo. Studying the murine meniscus as the model tissue, we showed that fibrocartilage PCM contains thinner, random collagen fibrillar networks that entrap proteoglycans, a structure distinct from the densely packed, highly aligned collagen fibers in the bulk extracellular matrix (ECM). In comparison to the ECM, the PCM has a lower modulus and greater isotropy, but similar relative viscoelastic properties. In Col5a1+/D menisci, the reduction of collagen V, a minor collagen localized in the PCM, resulted in aberrant fibril thickening with increased heterogeneity. Consequently, the PCM exhibited a reduced modulus, loss of isotropy and faster viscoelastic relaxation. This disrupted PCM contributes to perturbed mechanotransduction of resident meniscal cells, as illustrated by reduced intracellular calcium signaling, as well as upregulated biosynthesis of lysyl oxidase and tenascin C. When cultured in vitro, Col5a1+/D meniscal cells synthesized a weakened nascent PCM, which had inferior properties towards protecting resident cells against applied tensile stretch. These findings underscore the PCM as a distinctive microstructure that governs fibrocartilage mechanobiology, and highlight the pivotal role of collagen V in PCM function. Targeting the PCM or its molecular constituents holds promise for enhancing not only meniscus regeneration and osteoarthritis intervention, but also addressing diseases across various fibrocartilaginous tissues.

bioengineering↗

bioRxiv2024

In silico generation and augmentation of regulatory variants from massively parallel reporter assay using conditional variational autoencoder

Predicting the functional consequences of genetic variants in non-coding regions is a challenging problem. Massively parallel reporter assays (MPRAs), which are an in vitro high-throughput method, can simultaneously test thousands of variants by evaluating the existence of allele specific regulatory activity. Nevertheless, the identified labelled variants by MPRAs, which shows differential allelic regulatory effects on the gene expression are usually limited to the scale of hundreds, limiting their potential to be used as the training set for achieving a robust genome-wide prediction. To address the limitation, we propose a deep generative model, MpraVAE, to in silico generate and augment the training sample size of labelled variants. By benchmarking on several MPRA datasets, we demonstrate that MpraVAE significantly improves the prediction performance for MPRA regulatory variants compared to the baseline method, conventional data augmentation approaches as well as existing variant scoring methods. Taking autoimmune diseases as one example, we apply MpraVAE to perform a genome-wide prediction of regulatory variants and find that predicted regulatory variants are more enriched than background variants in enhancers, active histone marks, open chromatin regions in immune-related cell types, and chromatin states associated with promoter, enhancer activity and binding sites of cMyC and Pol II that regulate gene expression. Importantly, predicted regulatory variants are found to link immune-related genes by leveraging chromatin loop and accessible chromatin, demonstrating the importance of MpraVAE in genetic and gene discovery for complex traits.

bioinformatics↗

bioRxiv2024

GeneRAG: Enhancing Large Language Models with Gene-Related Task by Retrieval-Augmented Generation

Large Language Models (LLMs) like GPT-4 have revolutionized natural language processing and are used in gene analysis, but their gene knowledge is incomplete. Fine-tuning LLMs with external data is costly and resource-intensive. Retrieval-Augmented Generation (RAG) integrates relevant external information dynamically. We introduce GO_SCPLOWENEC_SCPLOWRAG, a frame-work that enhances LLMs gene-related capabilities using RAG and the Maximal Marginal Relevance (MMR) algorithm. Evaluations with datasets from the National Center for Biotechnology Information (NCBI) show that GO_SCPLOWENEC_SCPLOWRAG outperforms GPT-3.5 and GPT-4, with a 39% improvement in answering gene questions, a 43% performance increase in cell type annotation, and a 0.25 decrease in error rates for gene interaction prediction. These results highlight GO_SCPLOWENEC_SCPLOWRAGs potential to bridge a critical gap in LLM capabilities for more effective applications in genetics.

bioinformatics↗

bioRxiv2024

YAP inhibits NF-κB signaling and ccRCC growth by opposing p65-ZHX2 cooperativity

The prevailing view in the cancer field is that Hippo signaling pathway functions as a tumor suppressor pathway by blocking the oncogenic potential of the pathway effectors Yes1 associated transcriptional regulator (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ). However, YAP can also function as a context-dependent tumor suppressor in several types of cancer including clear cell renal cell carcinomas (ccRCC). We find that, in additional to inhibiting hypoxia-inducible factor 2 (HIF2), a major oncogenic driver in Von Hippel-Lindau (VHL)-/- ccRCC, YAP also blocks nuclear factor {kappa}B (NF-{kappa}B) signaling in ccRCC to inhibit cancer cell growth under conditions where HIF2 is dispensable. Mechanistically, YAP inhibits the expression of Zinc fingers and homeoboxes 2 (ZHX2), a VHL substrate and critical co-factor of NF-{kappa}B in ccRCC. Furthermore, YAP competes with ZHX2 for binding to the NF-{kappa}B subunit p65. Consequently, elevated nuclear YAP blocks the cooperativity between ZHX2 and the NF-{kappa}B subunit p65, leading to diminished NF-{kappa}B target gene expression. Pharmacological inhibition of Hippo kinase blocked NF-{kappa}B transcriptional program and suppressed ccRCC cancer cell growth, which can be rescued by overexpression of ZHX2 or p65. Our study uncovers a crosstalk between the Hippo and NF-{kappa}B/ZHX2 pathways and its involvement in ccRCC growth inhibition, suggesting that targeting the Hippo pathway may provide a therapeutical opportunity for ccRCC treatment.

cancer biology↗

bioRxiv2024

A host enzyme reduces non-alcoholic fatty liver disease by inactivating intestinal lipopolysaccharide

The incidence of Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) has been increasing world-wide. Since gut-derived bacterial lipopolysaccharides (LPS) can travel via the portal vein to the liver and play an important role in producing hepatic pathology, it seemed possible that (1) LPS stimulates hepatic cells to accumulate lipid, and (2) inactivating LPS can be preventive. Acyloxyacyl hydrolase (AOAH), the eukaryotic lipase that inactivates LPS and oxidized phospholipids, is produced in the intestine, liver, and other organs. We fed mice either normal chow or a high-fat diet for 28 weeks and found that Aoah-/- mice accumulated more hepatic lipid than did Aoah+/+ mice. In young mice, before increased hepatic fat accumulation was observed, Aoah-/-mouse livers increased their abundance of Sterol Regulatory Element-Binding Protein 1 (SREBP1) and the expression of its target genes that promote fatty acid synthesis. Aoah-/- mice also increased hepatic expression of CD36 and Fabp3, which mediate fatty acid uptake, and decreased expression of fatty acid oxidation-related genes Acot2 and Ppar-. Our results provide evidence that increasing AOAH abundance in the gut, bloodstream and/or liver may be an effective strategy for preventing or treating MASLD.

immunology↗

bioRxiv2024

Comprehensive mapping and modelling of the rice regulome landscape unveils the regulatory architecture underlying complex traits

Unraveling the regulatory mechanisms that govern complex traits is pivotal for advancing crop improvement. Here we present a comprehensive regulome atlas for rice (Oryza sativa), charting the chromatin accessibility across 23 distinct tissues from three representative varieties. Our study uncovers 117,176 unique open chromatin regions (OCRs), accounting for [~]15% of the rice genome, a notably higher proportion compared to previous reports in plants. Integrating RNA-seq data from matched tissues, we confidently predict 59,075 OCR-to-gene links, with enhancers constituting 69.54% of these associations, including many known enhancer-to-gene links. Leveraging this resource, we re-evaluate genome-wide association study results and discover a previously unknown function of OsbZIP06 in seed germination, which we subsequently confirm through experimental validation. We optimize deep learning models to decode regulatory grammar, achieving robust modeling of tissue-specific chromatin accessibility. This approach allows to predict cross-variety regulatory dynamics from genomic sequences, shedding light on the genetic underpinnings of cis-regulatory divergence and morphological disparities between varieties. Overall, our study establishes a foundational resource for rice functional genomics and precision molecular breeding, providing valuable insights into regulatory mechanisms governing complex traits.

genomics↗

bioRxiv2024

Wnt signaling dosage controlled by a Ctnnb1 enhancer balances homeostasis and tumorigenesis of intestinal epithelia

The {beta}-catenin-dependent canonical Wnt signaling is pivotal in organ development, tissue homeostasis, and cancer. Here we identified an upstream enhancer of Ctnnb1 - the coding gene for {beta}-catenin, named ieCtnnb1 (intestinal enhancer of Ctnnb1), which is crucial for intestinal homeostasis. ieCtnnb1 is predominantly active in the base of small intestinal crypts and throughout the epithelia of large intestine. Knockout of ieCtnnb1 led to a reduction in Ctnnb1 transcription, compromising the canonical Wnt signaling in intestinal crypts. Single-cell sequencing revealed that ieCtnnb1 knockout altered epithelial compositions and potentially compromised functions of small intestinal crypts. While deletion of ieCtnnb1 hampered epithelial turnovers in physiologic conditions, it prevented occurrence and progression of Wnt/{beta}-catenin-driven colorectal cancers. Human ieCTNNB1 drove reporter gene expression in a pattern highly similar to mouse ieCtnnb1. ieCTNNB1 contains a single-nucleotide polymorphism associated with CTNNB1 expression levels in human gastrointestinal epithelia. The enhancer activity of ieCTNNB1 in colorectal cancer tissues was stronger than that in adjacent normal tissues. HNF4 and phosphorylated CREB1 were identified as key trans-factors binding to ieCTNNB1 and regulating CTNNB1 transcription. Together, these findings unveil an enhancer-dependent mechanism controlling the dosage of Wnt signaling and homeostasis in intestinal epithelia.

cell biology↗

bioRxiv2024

Deep generative models generate mRNA sequences with enhanced translation capacity and stability

Despite the tremendous success of messenger RNA (mRNA) COVID-19 vaccines, the extension of this modality to a broader spectrum of diseases necessitates substantial enhancements, particularly in the design of mRNAs with elevated expression levels and extended durability. Here we present GEMORNA, a deep generative model designed to generate novel mRNA coding sequences (CDSs) and untranslated regions (UTRs) with superior translation capacity, comparable to the sophisticated task of language translation and free-form poetry composition with accurate grammar and semantics. Our AI model was trained on an extensive collection of RNA sequences from diverse families, further enhanced with labeled data to refine its performance. Remarkably, we demonstrate that our AI-generated mRNAs exhibited 8.2-fold and 15.9-fold increases in firefly luciferase expression compared to benchmark mRNAs in two different cell types. Additionally, Our AI- designed COVID-19 mRNA vaccine elicited a 4-fold increase in anti-COVID antibody titer in mice relative to BNT162b2. Furthermore, GEMORNAs versatility extends to circular mRNA design, which we facilitated a 27-fold increase in human erythropoietin protein expression in vivo than a systematically optimized benchmark sequence. We also created circular mRNAs with substantial improvements in expression levels, durability and anti-tumor cell cytotoxicity in mRNA-transduced CAR-T cells compared with an experimentally validated benchmark. In summary, GEMORNA generates novel mRNA sequences with significant performance improvements and has the potential to enable a wide range of therapeutic and vaccine applications.

synthetic biology↗

bioRxiv2024

Prime editor-based high-throughput screening reveals functional synonymous mutations in the human genome

Synonymous mutations are generally considered neutral, while their roles in the human genome remain largely unexplored. Herein, we employed the PEmax system to create a library of 297,900 epegRNAs and performed extensive screening to identify synonymous mutations that impact cell fitness. While most synonymous mutations are neutral, we found that some can elicit phenotypic effects. By developing a specialized machine learning tool, we uncovered their impact on various biological processes such as mRNA splicing and transcription, supported by multifaceted experimental evidence. Notably, synonymous mutations can alter RNA folding and affect translation, as demonstrated by PLK1_S2. By integrating screening data with our model, we successfully predicted clinically deleterious synonymous mutations. This research deepens our understanding of synonymous mutations and provides insights for clinical disease studies.

genetics↗

bioRxiv2024

Liver-specific Mettl14 deletion induces nuclear heterotypia and dysregulates RNA export machinery

Modification of RNA with N6-methyladenosine (m6A) has gained attention in recent years as a general mechanism of gene regulation. In the liver, m6A, along with its associated machinery, has been studied as a potential biomarker of disease and cancer, with impacts on metabolism, cell cycle regulation, and pro-cancer state signaling. However these observational data have yet to be causally examined in vivo. For example, neither perturbation of the key m6A writers Mettl3 and Mettl14, nor the m6A readers Ythdf1 and Ythdf2 have been thoroughly mechanistically characterized in vivo as they have been in vitro. To understand the functions of these machineries, we developed mouse models and found that deleting Mettl14 led to progressive liver injury characterized by nuclear heterotypia, with changes in mRNA splicing, processing and export leading to increases in mRNA surveillance and recycling.

molecular biology↗

bioRxiv2024

Inferring single-cell spatial gene expression with tissue morphology via explainable deep learning

Deep learning models trained with spatial omics data uncover complex patterns and relationships among cells, genes, and proteins in a high-dimensional space. State-of-the-art in silico spatial multi-cell gene expression methods using histological images of tissue stained with hematoxylin and eosin (H&E) allow us to characterize cellular heterogeneity. We developed a vision transformer (ViT) framework to map histological signatures to spatial single-cell transcriptomic signatures, named SPiRiT. SPiRiT predicts single-cell spatial gene expression using the matched H&E image tiles of human breast cancer and whole mouse pup, evaluated by Xenium (10x Genomics) datasets. Importantly, SPiRiT incorporates rigorous strategies to ensure reproducibility and robustness of predictions and provides trustworthy interpretation through attention-based model explainability. SPiRiT model interpretation revealed the areas, and attention details it uses to predict gene expressions like marker genes in invasive cancer cells. In an apple-to-apple comparison with ST-Net, SPiRiT improved the predictive accuracy by 40%. These gene predictions and expression levels were highly consistent with the tumor region annotation. In summary, SPiRiT highlights the feasibility to infer spatial single-cell gene expression using tissue morphology in multiple-species.

bioinformatics↗

bioRxiv2024

PFS alleviates bone destruction in collagen-induced arthritis mice associated with macrophage polarization

Periploca forrestii Schltr is a clinical traditional Chinese medicine for the treatment of Rheumatoid arthritis (RA). This study aimed to investigate effects of Periploca forrestii Schltr saponin (PFS) on bone destruction and macrophage polarization in arthritis model mice and to explore its possible mechanism. Arthritis was induced in two species, BALB/c and C57BL/6 mice, by immunization with type II chicken collagen. The arthritic mice were administered PFS for four weeks. The hindfeet, blood and spleen were harvested. Molecular expression was determined by ELISA, RT-PCR and immunoblotting. PFS treatment resulted in a significant reduction in paw swelling in both species of mice. PFS also reduced cartilage destruction and infiltration of osteoclasts in BALB/c mice. Furthermore, it decreased the levels of M1 macrophage cytokines while increasing the levels of M2 macrophage cytokines in the paw and plasma. Micro-CT results in C57BL/6 mice showed that PFS attenuated microstructural damage in bone tissue. PFS inhibited CD68 and affected the expression of M1 macrophage factors such as CCL-2, TLR4, and IL-1{beta} in the mouse paw. In addition, PFS treatment increased the M2 macrophage factor CD206 and CD163. PFS inhibits the activation of ERK, JNK, and p38 and the expression of transcription factors, including STAT3, p65, and c-Fos. PFS may modulate pleiotropic macrophage polarization and thus play an ameliorative role in bone damage, therefore PFS may be an effective alternative drug for the treatment of RA.

immunology↗

bioRxiv2024

Frontal Cortex Hyperactivation and Gamma Desynchrony in Fragile X Syndrome: Correlates of Auditory Hypersensitivity

Fragile X syndrome (FXS) is an X-linked disorder that often leads to intellectual disability, anxiety, and sensory hypersensitivity. While sound sensitivity (hyperacusis) is a distressing symptom in FXS, its neural basis is not well understood. It is postulated that hyperacusis may stem from temporal lobe hyperexcitability or dysregulation in top-down modulation. Studying the neural mechanisms underlying sound sensitivity in FXS using scalp electroencephalography (EEG) is challenging because the temporal and frontal regions have overlapping neural projections that are difficult to differentiate. To overcome this challenge, we conducted EEG source analysis on a group of 36 individuals with FXS and 39 matched healthy controls. Our goal was to characterize the spatial and temporal properties of the response to an auditory chirp stimulus. Our results showed that males with FXS exhibit excessive activation in the frontal cortex in response to the stimulus onset, which may reflect changes in top-down modulation of auditory processing. Additionally, during the chirp stimulus, individuals with FXS demonstrated a reduction in typical gamma phase synchrony, along with an increase in asynchronous gamma power, across multiple regions, most strongly in temporal cortex. Consistent with these findings, we observed a decrease in the signal-to-noise ratio, estimated by the ratio of synchronous to asynchronous gamma activity, in individuals with FXS. Furthermore, this ratio was highly correlated with performance in an auditory attention task. Compared to controls, males with FXS demonstrated elevated bidirectional frontotemporal information flow at chirp onset. The evidence indicates that both temporal lobe hyperexcitability and disruptions in top-down regulation play a role in auditory sensitivity disturbances in FXS. These findings have the potential to guide the development of therapeutic targets and back-translation strategies.

neuroscience↗

bioRxiv2024

Occurrence, risk assessment of antibiotics and antimicrobial resistance in Escherichia coli in typical rivers of Sichuan

Worldwide interest has been generated by the presence and distribution of antibiotics and antibiotic resistance genes (ARGs) in rivers. However, there was a dearth of research on the contamination of Sichuan provinces typical rivers with antibiotics. In this study, the residual level of antibiotics in 42 national/provincial sites of 9 rivers was analyzed by UPLC-MS/MS, the ecological risk level was evaluated using risk assessment method, and the drug resistance of E. coli in water was evaluated by Kirby-Bauer method. Redundancy analysis demonstrated how residual antibiotics affect the structure of the microbial community in the Minjiang River basin (RDA). Nine rivers all contained antibiotics. Among them, the MinJiang, TuoJiang, and JiaLingJiang rivers were severely contaminated with antibiotic concentrations ranging from 0.29 to 2233.71 ng/L. The Sichuan Basins antibiotic pollution level was significantly higher when compared to other Sichuan zones, which was consistent with the regions high population density. Additionally, it was discovered that 9.77% of the E. coli isolated from 9 rivers had antibiotic resistance, and more than 5.8% of them had multidrug resistance. Moreover, Norfloxacin, amoxicillin, ampicillin, and tetracycline were the main risk factors for high ecological risk in 26 of the 42 monitoring sites. Additionally, there is a strong correlation between the microbial community change and residual antibiotic. These results offered some reference information regarding the distribution of antibiotics and ARGs in typical rivers in the Chinese province of Sichuan, and this study showed that more attention needs to be paid to antibiotic pollution in Sichuans typical rivers.

microbiology↗

bioRxiv2024

Membrane binding properties of the cytoskeletal protein bactofilin

Bactofilins are a widespread family of cytoskeletal proteins with important roles in bacterial morpho-genesis, chromosome organization and motility. They polymerize in a nucleotide-independent manner, forming non-polar filaments that are typically associated with the cytoplasmic membrane. Membrane binding was suggested to be mediated by a short N-terminal peptide, but the underlying mechanism and the conservation of this interaction determinant among bacteria remain unclear. Here, we use the bacto-filin homolog BacA of the stalked bacterium Caulobacter crescentus as a model to analyze the membrane-binding behavior of bactofilins. Based on site-directed mutagenesis of the N-terminal region, we identify the full membrane-targeting sequence of BacA (MFSKQAKS) and pinpoint amino acid residues that are critical for its function in vivo and in vitro. Molecular dynamics simulations then provide detailed insight into the molecular mechanism underlying the membrane affinity of this peptide. Collectively, these analyses reveal a delicate interplay between the water exclusion of hydrophobic N-terminal residues, the arrangement of the peptide within the membrane and the electrostatic attraction between positively charged groups in the peptide and negative charges in the phospholipid molecules. A comprehensive bio-informatic analysis shows that the composition and properties of the membrane-targeting sequence of BacA are conserved in numerous bactofilin homologs from diverse bacterial phyla. Importantly, our findings reveal cooperative effects between the membrane-binding and polymerization activities of BacA. Moreover, they demonstrate that both of these activities critically contribute to the recruitment of the BacA client protein PbpC, a membrane-bound cell wall synthase that uses a conserved peptide in its N-terminal cytoplasmic tail to interact with BacA assemblies. Finally, we show that PbpC can functionally replace the endogenous membrane-targeting sequence of BacA when provided at elevated levels in trans, indicating that client proteins can make a significant contribution to the membrane association of bacto-filin polymers. Together, these results unravel the mechanistic underpinnings of membrane binding by bactofilin homologs, thereby illuminating a previously obscure but important aspect in the biology of this cytoskeletal protein family.

microbiology↗