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Biology subjects

Jiang, J.

Publications and source records attributed to Jiang, J..

At least 145 records · Page 8Linked to original sources

A Kinetic Scout Approach Accelerates Targeted Protein Degrader Development

Bifunctional molecules such as targeted protein degraders induce proximity to promote gain-of-function pharmacology. These powerful approaches have gained broad traction across academia and the pharmaceutical industry, leading to an intensive focus on strategies that can accelerate their identification and optimization. We and others have previously used chemical proteomics to map degradable target space, and these datasets have been used to develop and train multiparameter models to extend degradability predictions across the proteome. In this study, we now turn our attention to develop generalizable chemistry strategies to accelerate the development of new bifunctional degraders. We implement lysine-targeted reversible-covalent chemistry to rationally tune the binding kinetics at the protein-of-interest across a set of 25 targets. We define an unbiased workflow consisting of global proteomics analysis, IP/MS of ternary complexes and the E-STUB assay, to mechanistically characterize the effects of ligand residence time on targeted protein degradation and formulate hypotheses about the rate-limiting step of degradation for each target. Our key finding is that target residence time is a major determinant of degrader activity, and this can be rapidly and rationally tuned through the synthesis of a minimal number of analogues to accelerate early degrader discovery and optimization efforts.

pharmacology and toxicology↗

Phosphorylation-induced SUMOylation promotes Ulk4 condensation at ciliary tip to transduce Hedgehog signal

Hedgehog (Hh) signaling controls embryonic development and adult tissue homeostasis through the Gli family of transcription factors. In vertebrates, Hh signal transduction depends on the primary cilium where Gli is thought to be activated at the ciliary tip, but the underlying mechanism has remained poorly understood. Here we provide evidence that two Unc-51-like kinase (Ulk) family members Stk36 and Ulk4 regulate Gli2 ciliary tip localization and activation through phosphorylation and SUMOylation-mediated condensation in response to Shh. We find that Stk36-mediated phosphorylation of Ulk4 promotes its SUMOylation in response to Shh, and the subsequent interaction between SUMO and a SUMO-Interacting-Motif (SIM) in the C-terminal region of Ulk4 drives Ulk4 self-assembly to form biomolecular condensates that also recruit Stk36 and Gli2. SUMOylation or SIM-deficient Ulk4 failed to accumulate at ciliary tip to activate Gli2 whereas phospho-mimetic mutation of Ulk4 sufficed to drive Ulk4/Stk36/Gli2 condensation at ciliary tip, leading to constitutive Shh pathway activation in a manner dependent on Ulk4 SUMOylation. Taken together, our results suggest that phosphorylation-dependent SUMOylation of Ulk4 promotes kinase-substrate condensation at ciliary tip to transduce the Hh signal.

cell biology↗

A circular engineered sortase for interrogating histone H3 in chromatin

Reversible modification of the histone H3 N-terminal tail is critical in regulating chromatin structure, gene expression, and cell states, while its dysregulation contributes to disease pathogenesis. Understanding the crosstalk between H3 tail modifications in nucleosomes constitutes a central challenge in epigenetics. Here we describe an engineered sortase transpeptidase, cW11, that displays highly favorable properties for introducing scarless H3 tails onto nucleosomes. This approach significantly accelerates the production of both symmetrically and asymmetrically modified nucleosomes. We demonstrate the utility of asymmetrically modified nucleosomes produced in this way in dissecting the impact of multiple modifications on eraser enzyme processing and molecular recognition by a reader protein. Moreover, we show that cW11 sortase is very effective at cutting and tagging histone H3 tails from endogenous histones, facilitating multiplex "cut-and-paste" middle down proteomics with tandem mass tags. This cut-and-paste proteomics approach permits the quantitative analysis of histone H3 modification crosstalk after treatment with different histone deacetylase inhibitors. We propose that these chemoenzymatic tail isolation and modification strategies made possible with cW11 sortase will broadly power epigenetics discovery and therapeutic development.

biochemistry↗

ADAR1 orchestrates the ZBP1-mediated PANoptosis and heart transplant rejection

BackgroundPANoptosis is an integrated form of cell death that combines features of pyroptosis, apoptosis, and necroptosis and is regulated by a complex network of signaling proteins. The roles of ADAR1 (adenosine deaminase acting on RNA 1) and RIPK1 (receptor-interacting serine/threonine-protein kinase 1) in orchestrating the ZBP1 (Z-DNA binding protein 1)-RIPK3 complex to mediate PANoptosis is not fully understood, particularly in the context of heart transplantation. ObjectiveThis study investigated how ADAR1 and RIPK1 coordinate the activation of the ZBP1-RIPK3 complex to mediate PANoptosis and its implications in mouse heart transplantation. MethodsUsing both in vitro and in vivo models, we analyzed the interactions between ADAR1, RIPK1, ZBP1, and RIPK3. We employed western blotting, and siRNA to elucidate the dynamics of these interactions. Additionally, we assessed the impact of ZBP1 on mouse heart transplantation outcomes. ResultsOur studies revealed that ADAR1 regulates the activation of the ZBP1-RIPK3 complex for PANoptosis. The interaction of ADAR1 with ZBP1 protected against Z-DNA-induced cell death by limiting activations of ZBP1 and RIPK3. In mouse heart transplantation study, we found that ZBP1 and its ligand Z-DNA/Z-RNA were significantly increased in the graft post-transplantation. Furthermore, ZBP1 deficiency in the heart graft inhibited cardiac PANoptosis, attenuated acute graft injury, and induced long-term graft survival. ConclusionThis study elucidates the role of ADAR1 in ZBP1-mediated PANoptosis. Inhibition of ZBP1 can prevent heart graft injury and rejection. Understanding these mechanisms provides valuable insights into the regulation of cell death and may inform the development of novel therapeutic strategies to improve transplant outcomes.

molecular biology↗

MorphLink: Bridging Cell Morphological Behaviors and Molecular Dynamics in Multi-modal Spatial Omics

Multi-modal spatial omics data are invaluable for exploring complex cellular behaviors in diseases from both morphological and molecular perspectives. Current analytical methods primarily focus on clustering and classification, and do not adequately examine the relationship between cell morphology and molecular dynamics. Here, we present MorphLink, a framework designed to systematically identify disease-related morphological-molecular interplays. MorphLink has been evaluated across a wide array of datasets, showcasing its effectiveness in extracting and linking interpretable morphological features with various molecular measurements in multi-modal spatial omics analyses. These linkages provide a transparent depiction of cellular behaviors that drive transcriptomic heterogeneity and immune diversity across different regions within diseased tissues, such as cancer. Additionally, MorphLink is scalable and robust against cross-sample batch effects, making it an efficient method for integrative spatial omics data analysis across samples, cohorts, and modalities, and enhancing the interpretation of results for large-scale studies.

bioinformatics↗

Low-cost and highly efficient generation of near-complete bacterial pathogen genomes by TELL-Seq

Recent evidences suggest that de novo genome assembly can provide additional insights into genomic variation landscape beyond short-read NGS analyses. Despite the advent of longread sequencing technologies, generating high-quality bacterial genome assemblies remains expensive and requires high-quality and large quantities of DNA. TELL-Seq, an emerging linked-read technology, has been reported as a low-cost alternative for producing nearcomplete genome assembly in certain bacterial species. However, a systematic assessment of its performance and characteristics in de novo bacterial genome assembly has not yet been conducted. To address this, we benchmarked TELL-Seq using a set of clinical and standard bacterial pathogens with a wide range of genome size (2.0 6.4 Mbp), GC-content (32% - 68%), genome complexity (mappability from 0.15 to 0.60) and Gram types. Our findings indicate that, with 1/6 cost and 1/15,000 of DNA compared to PacBio HiFi, TELL-Seq could generate as high quality near-complete bacterial genome assemblies. The optimal depth for assembly is around 200x, as increased depth improves contiguity and completeness, though quality plateaus at 250x. In general, genome complexity was significantly correlated with assembly quality, but GC-content was not. Nevertheless, genomes with extreme GC-content may require higher depths for accurate assembly. Our study suggests that TELL-Seq could be a scalable method for large-scale bacterial genomic surveys. The data generated from this study could serve as a benchmark dataset for further algorithm development. Impact StatementAn increasing body of literature have shown that de novo genome assembles could provide additional insights into genomic variation beyond standard short-read technologies. Its particularly useful in clinical and epidemiological studies of bacteria, due to high variable nature of their genomes. Although great advances have been made in long-read sequencing technology, its still expensive with high requirement over sample DNAs quality and quantity, limiting its adoption in large-scale studies or surveys. Linked-read technology is an inexpensive alternative which used single molecule barcoding to mark origin of reads for better scaffolding of contigs assembled from normal short reads. TELL-Seq, as one of these promising technologies, was reported to be able to inexpensively and efficiently generate near-complete bacterial de novo genomic assemblies with low DNA inputs. Theres not yet a systematic benchmarking of this technology in bacterial pathogens. In this study, a set of clinically important bacterial pathogens with a wide spectrum of GC-content, genome size, genome complexity, and Gram Type were used to investigate the performance of TELL-Seq technology in de novo genome assembly. We found that, with about 1/6 of cost and 1/15000 of DNA quantity, it could generate comparable de novo assemblies compared to standard reference genomes or PacBio HiFi assemblies, while beating conventional short-read assemblies. We found several key factors, such as genome complexity, and sequencing depth, which would impact the quality of the assembly. Our study suggests that a sequencing depth of 200x is sufficient to achieve satisfactory results. Our study has revealed characteristics of this technology in bacterial genome assembly and paved the way for its large-scale application in clinical or epidemiological surveys. Data SummaryO_LIRaw sequencing data for all isolates have been deposited to SRA, accessible through these NCBI BioProject PRJNA1133244. C_LIO_LIA full list of SRA BioSample accession numbers are available in Tab S5. C_LIO_LIAssemblies and analyses companion this paper is available at: https://github.com/x-lab/tellseq_bacteria C_LI

bioinformatics↗

Fibroblastic FLT3L supports lymph node dendritic cells in the interfollicular niche

Dendritic cell (DC) homeostasis is maintained in secondary lymphoid organs (SLOs) by Fms-like tyrosine kinase 3 ligand (FLT3L). The specific niche providing this DC growth factor within human and mouse SLOs is unclear. Here, we show that Gremlin1 (Grem1)-expressing lymph node fibroblastic reticular cells (FRCs) support DC homeostasis via provision of FLT3L. Grem1 FRCs co-localize with DCs and express FLT3L in human and mouse lymph nodes. Using a new genetic model, we provide evidence that FLT3L produced by GREM1 FRCs maintains lymph node preDCs, cDCs, and plasmacytoid DCs (pDCs). Spatial transcriptomics and cytofluorometry reveal that Grem1 FRC-derived FLT3L supports not only proliferation, but also survival of lymph node cDCs within the interfollicular zone (IFZ). Functionally, loss of Grem1 FRC-derived FLT3L impairs cDC priming of antigen-specific T cell responses. These findings provide key mechanistic insights underlying stromal cell support of DC homeostasis and function.

immunology↗

Expression and characterization of the complete cyanophage genome PP in the heterologous host Synechococcus elongatus PCC 7942

Cyanophages are considered a promising biological management option for treating cyanobacterial blooms. Broadening the host range of cyanophages and/or shortening the lysis cycle by designing and synthesizing artificial cyanophages are potential strategies to enhance their effectiveness and efficiency. However, the rescue of artificial cyanophage genomes remains unexplored. In this study, we achieved the integration of a full-length cyanophage genome, PP, which originally infects Plectonema boryanum FACHB-240, into the model cyanobacterium Synechococcus elongatus PCC 7942. Since the integration of these large fragments ([~]42 kb) into cyanobacteria depended on conjugation via Escherichia coli, the toxic open reading frames (ORFs) of PP to E. coli were first identified, leading to the identification of toxic ORF6, ORF11, and ORF22. The original PP genome was then rearranged, and the three toxic ORFs were controlled using a tandem induction switch. The full length of the PP genome was integrated into the genome of S. elongatus PCC 7942 via two rounds of homologous recombination. Interestingly, compared to the control strain, the integration of the PP genome decreased photosynthesis and carbon fixation in S. elongatus PCC 7942, exhibiting cyanophage-like behavior. Transcriptomic analysis revealed that 32 of the 41 ORFs of the PP genome were transcribed in S. elongatus PCC 7942, significantly altering the energy metabolism and carbon fixation pathways. These influences were further demonstrated using metabolomics. This study provides a comprehensive approach for the artificial design and integration of cyanophage genomes in cyanobacteria, laying the foundation for their real rescue in the future.

synthetic biology↗

Substrate specificity and protein stability drive the divergence of plant-specific DNA methyltransferases

DNA methylation is an important epigenetic mechanism essential for transposon silencing and genome integrity. Across evolution, the substrates of DNA methylation have diversified between kingdoms to account for genome complexity. In plants, Chromomethylase3 (CMT3) and CMT2 are the major methyltransferases mediating CHG and CHH methylation, respectively. However, how these two enzymes diverge on substrate specificities during evolution remains unknown. Here, we reveal that CMT2 originates from a duplication of the evolutionarily more ancient CMT3 in flowering plants. Lacking a key arginine residue recognizing CHG in CMT2 impairs its CHG methylation activity in most flowering plants. An engineered V1200R mutation empowers CMT2 to restore both CHG and CHH methylation in Arabidopsis cmt2cmt3 mutant, testifying a loss-of-function effect for CMT2 after [~]200 million years of evolution. Interestingly, CMT2 has evolved a long and unstructured N-terminus critical for balancing protein stability, especially under heat stress. Furthermore, CMT2 N-terminus is plastic and can be tolerant to various natural mutations. Together, this study reveals the mechanism of chromomethylase divergence for context-specific DNA methylation in plants and sheds important lights on DNA methylation evolution and function.

plant biology↗

Acute BRCAness Induction and AR Signaling Blockage through CDK12/7/9 Degradation Enhances PARP Inhibitor Sensitivity in Prostate Cancer

Current treatments for advanced prostate cancer (PCa) primarily target the androgen receptor (AR) pathway. However, the emergence of castration-resistant prostate cancer (CRPC) and resistance to AR pathway inhibitors (APSIs) remains ongoing challenges. Here, we present BSJ-5-63, a novel proteolysis-targeting chimera (PROTAC) targeting cyclin-dependent kinases (CDKs) CDK12, CDK7, and CDK9, offering a multi-pronged approach to CRPC therapy. BSJ-5-63 degrades CDK12, diminishing BRCA1 and BRCA2 expression and inducing a sustained "BRCAness" state. This sensitizes cancer cells to PARP inhibitors (PARPis) regardless of their homologous recombination repair (HRR) status. Furthermore, CDK7 and CDK9 degradation attenuates AR signaling, enhancing its therapeutic efficacy. Preclinical studies, including both in vitro and in vivo CRPC models, demonstrate that BSJ-5-63 exerts potent anti-tumor activity in both AR-positive and AR-negative setting. This study introduces BSJ-5-63 as a promising therapeutic agent that addresses both DNA repair and AR signaling mechanisms, with potential benefits for a board patient population.

cancer biology↗

A chromosome-level genome assembly of Dracaena cambodiana and comparative genomics analysis highlights the distinct biological features of two resource species of dragon's blood

This study reports a chromosome-level genome for Dracaena cambodiana, one of two typical dracaena species in China. This work will help to deepen the understanding of the dracaena species and the conservation and development of plant resources. The final assembly consisted of 54 scaffolds, spanning 1.08 Gb, with a scaffold N50 size of 52.29 Mb, encoded 36860 predicted protein-coding genes. A total of 1,064,810,157 bp of genome sequences were located on 20 chromosomes (2n = 40), accounting for 98.46%. We investigate the possible mechanisms of the longevity of dracaena, the longest-lived plant in the world, which involve DNA repair and post-translational modification. We also performed comparative genomic analysis of the previously assembled genome of Dracaena cochinchinesis with this genome, and found that the two involved interaction of plant-pathogen interaction and ubiquitin mediated proteolysis, which may reveal why Dracaena has environmental adaptability and longevity characteristics.

genomics↗

Adaptive Container Service: a New Paradigm for Robust and Optimized Bioinformatics Workflow Deployment in the Cloud.

We propose Adaptive Container Service (ACS), a new paradigm for deploying bioinformatics workflows in cloud computing environments. By encapsulating the entire workflow within a single virtual container, combined with automatic workflow checkpointing and dynamic migration to appropriately scaled containers, ACS-based deployment demonstrates several key advantages over alternative strategies: it enables optimal resource provision to any workflow that comprise of multiple applications with diverse computing needs; it provides protection against application-agnostic out-of-memory (OOM) errors or spot instance interruptions; and it reduces efforts required for workflow development, optimization, and management because it runs workflows with minimal or no code modifications. Proof-of-concept experiments show that ACS avoided both under- and over-provisioning in monolithic single-container deployment. Despite being deployed as a single container, it achieved comparable resource utilization efficiency as optimized Nextflow-managed, multi-modular workflows. Analysis of over 18,000 workflow runs demonstrated that ACS can effectively reduce workflow failures by two-thirds. These findings suggest that ACS frees developers from navigating the complexity of deploying robust workflows and rightsizing compute resources in the cloud, leading to significant reduction in workflow development time and savings in cloud computing costs.

bioinformatics↗

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↗

Intra-genomic genes-to-genes correlation enables genome representaion

The bacterial pan-genome consists of core genes shared by all members of a taxonomy and accessory genes found in only a subset. The correlation among genes within the pan-genome could advance our understanding of evolution and tackle medical challenges. Here, we discovered a strong intra-genomic correlation among bacterial pan-genes within each of Escherichia coli, Listeria monocytogenes, Staphylococcus aureus, and Campylobacter jejuni. With a convolutional neural network assisted core genome knock-out simulation, we found that different combinations of fewer than 20 highly variable core genes could recover the sub-species type classified by complete core genome with accuracy >95%. This observation led us to test the genes-to-genes predictability: with more than 52,000 assemblies from each species, combinations of highly variable core genes could predict the sequence variants of other core genes (average accuracy >94%) within the same genome and could also predict sequence variants (average accuracy >91%) as well as the presence (average AUROC >0.91) of some accessory genes. Furthermore, combinations of highly variable core genes could also predict multiple antibiotic resistances (AUROC >0.80) in large published datasets of E. coli, S. aureus, and Mycobacterium tuberculosis. Collectively, we propose that genes within the same genome can strongly correlate with each other. Therefore, the strain phylogeny and the status of other genes could be uniformly represented by combinations of highly variable core genes, which could further represent certain phenotypes including in vitro resistance.

bioinformatics↗

ClpS directs degradation of primary N-end rule substrates in Mycolicibacterium smegmatis

Drug-resistant tuberculosis infections are a major threat to global public health. The essential mycobacterial ClpC1P1P2 protease has received attention as a prospective target for novel antibacterial therapeutics. However, efforts to probe its function in cells are constrained by our limited knowledge of its physiological proteolytic repertoire. Here, we interrogate the role of mycobacterial ClpS in directing N-end rule proteolysis by ClpC1P1P2 in Mycolicibacterium smegmatis. Binding assays demonstrate that mycobacterial ClpS binds canonical primary N-degrons (Leu, Phe, Tyr, Trp) with moderate affinity. N-degron binding restricts the conformational flexibility of a loop adjacent to the ClpS N-degron binding pocket and strengthens ClpS*ClpC1 binding affinity [~]30-fold, providing a mechanism for cells to prioritize N-end rule proteolysis when substrates are abundant. Proteolytic reporter assays in M. smegmatis confirm degradation of substrates bearing primary N-degrons, but suggest that secondary N-degrons are absence in mycobacteria. This work expands our understanding of the mycobacterial N-end rule pathway and identifies ClpS as a critical component for substrate specificity, providing insights that may support the development of improved Clp protease inhibitors.

biochemistry↗

Tripartite organization of brain state dynamics underlying spoken narrative comprehension

Speech comprehension involves the dynamic interplay of multiple cognitive processes, from basic sound perception, to linguistic encoding, and finally to complex semantic-conceptual interpretations. How the brain handles the diverse streams of information processing remains poorly understood. Applying Hidden Markov Modeling to fMRI data obtained during spoken narrative comprehension, we reveal that the whole brain networks predominantly oscillate within a tripartite latent state space. These states are respectively characterized by high activities in the sensory-motor (State #1), bilateral temporal (State #2), and DMN (State #3) regions, with State #2 acting as a transitional hub. The three states are selectively modulated by the acoustic, word-level semantic and clause-level semantic properties of the narrative. Moreover, the alignment with the best performer in brain state expression can predict participants narrative comprehension scores. These results are reproducible with different brain network atlas and generalizable to two datasets consisting of young and older adults. Our study suggests that the brain underlies narrative comprehension by switching through a tripartite state space, with each state probably dedicated to a specific component of language faculty, and effective narrative comprehension relies on engaging those states in a timely manner.

neuroscience↗

Identification and Characterization of the Lipoprotein N-acyltransferase in Bacteroides

Members of the Bacteroidota compose a large portion of the human gut microbiota, contributing to overall gut health via the degradation of various polysaccharides. This process is facilitated by lipoproteins, globular proteins anchored to the cell surface by a lipidated N-terminal cysteine. Despite their importance, lipoprotein synthesis by these bacteria is understudied. In E. coli, the -amino linked lipid of lipoproteins is added by the lipoprotein N-acyltransferase Lnt. Herein, we have identified a protein distinct from Lnt responsible for the same process in Bacteroides, named lipoprotein N-acyltransferase in Bacteroides (Lnb). Deletion of Lnb yields cells that synthesize diacylated lipoproteins, with impacts on cell viability and morphology, growth on polysaccharides, and protein composition of membranes and outer membrane vesicles (OMVs). Our results not only challenge the accepted paradigms of lipoprotein biosynthesis in Gram-negative bacteria, but also support the establishment of a new family of lipoprotein N-acyltransferases. SignificanceBacteroidota are key members of the human gut microbiota that influence human health by degrading polysaccharides. This degradation is achieved by a suite of lipoproteins, a class of membrane protein characterized by lipidation. Lipoprotein synthesis in Bacteroidota is understudied. Here, we used a genetic screen to identify gene(s) responsible for N-acylation, the last step in lipoprotein biosynthesis. Our screen identified the lipoprotein N-acyltransferase in Bacteroides (Lnb) that performs this step. We show that deletion of Lnb negatively affects cellular growth and ability to degrade polysaccharides, deepening our understanding of Bacteroidota and lipoproteins.

microbiology↗

Structural and Biophysical Dynamics of Fungal Plasma Membrane Proteins and Implications for Echinocandin Action in Candida glabrata

Fungal plasma membrane proteins represent key therapeutic targets for antifungal agents, yet their structure and spatial distribution in the native context remain poorly characterized. Herein, we employ an integrative multimodal approach to elucidate the structural and functional organization of plasma membrane protein complexes in Candida glabrata, focusing on prominent and essential membrane proteins, the polysaccharide synthase {beta}-(1,3)-glucan synthase (GS) and the proton pump Pma1. Cryo-electron tomography (cryo-ET) and live cell imaging reveal that GS and Pma1 are heterogeneously distributed into distinct plasma membrane microdomains. Treatment with caspofungin, an echinocandin antifungal that targets GS, alters the plasma membrane and disrupts the native distribution of GS and Pma1. Based on these findings, we propose a model for echinocandin action that considers how drug interactions with the plasma membrane environment lead to inhibition of GS. Our work underscores the importance of interrogating the structural and dynamic characteristics of fungal plasma membrane proteins in situ to understand function and facilitate precisely targeted development of novel antifungal therapies.

cell biology↗