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Mohammed, S.

Publications and source records attributed to Mohammed, S..

At least 19 recordsLinked to original sources

Hexosyl transfer via a covalent intermediate within a dual retaining and inverting enzyme

Bifunctional glycosyltransferases underpin biosynthesis of essential glycans, including bacterial capsular antigens, and eukaryotic glycosaminoglycans. Typically, these enzymes transfer hexose sugars from activated nucleotide-phosphate donors, forming new glycosidic bonds with either retention or inversion of anomeric stereochemistry. Retaining hexosyl transfer typically proceeds via non-covalent SNi-type pathways, but recent studies of octulosyl Kdo-transferases have reignited debate over covalent mechanisms. Here we comprehensively dissected the activity of the archetypal bifunctional glycosyltransferase PmHS2, providing X-ray structures of ligand complexes alongside atomistic simulations to delineate full substrate-to-product reaction trajectories. Combined computational, biochemical and evolutionary evidence suggests that PmHS2 retaining GlcNAc-transfer likely proceeds via a previously undescribed covalent mechanism, involving considerable assistance from departing nucleotide-phosphate rotation. In mapping reaction pathways, we also report the first example of a glycosyl donor substrate coopted as an acceptor, which enables enzymatic self-priming for polymerization. These new covalent and self-priming functionalities highlight unexplored routes to modulate or inhibit polysaccharide biosynthesis.

biochemistry↗

Design, Amino-Acid-Derived Analogues of FTY-720 and OSU-2S as PP2A Activators: Structure-Activity Relationships and Identification of Lead Compound XML-3D

Protein phosphatase 2A (PP2A) is a critical regulator of oncogenic signaling pathways, and pharmacological reactivation of PP2A through disruption of inhibitory protein interactions has emerged as a promising anticancer strategy. Although the sphingosine analogue FTY-720 and its derivative OSU-2S can restore PP2A activity, further structural diversification is needed to improve potency and expand structure-activity understanding. Here, we report the design, synthesis, and biological evaluation of three series of amino-acid-derived analogues incorporating tyrosine, homotyrosine, and tryptophan scaffolds. Docking models were used qualitatively to guide exploration of head-group functionality, hydrophobic tail variation, and stereochemical configuration; these models were hypothesis-generating and were not experimentally validated. Modular synthetic routes enabled efficient preparation of structurally diverse compounds from naturally occurring starting materials. Biological evaluation in leukemia and lymphoma cell lines revealed that hydrophobic tail length strongly influenced cytotoxic activity, while tryptophan-derived analogues were generally less potent than tyrosine-based scaffolds. Shortening the hydrophobic tail did not improve activity, contrary to the initial docking-based hypothesis. Stereochemical inversion at the amino alcohol head group yielded a lead compound, XML-3D, which demonstrated approximately two-fold enhanced cytotoxicity relative to FTY-720 and OSU-2S across leukemia cell lines (IC50 = 4.1, 1.8, and 1.5 uM in MV4-11, HL-60, and MEC-1 cells, respectively) and showed broader activity in mantle cell lymphoma lines (IC50 = 530 nM, 970 nM, and 110 nM in Jeko-1, Mino-1, and UPN1 cells). XML-3D induced increased PP2A phosphatase activity in cellular assays. Co-immunoprecipitation and pharmacological inhibition experiments were consistent with modulation of the PP2A/SET regulatory axis; however, direct binding measurements were not performed, and the mechanistic interpretation remains provisional. These findings suggest preliminary structure-activity relationships for amino-acid-derived PP2A modulators and identify stereochemical optimization as a productive direction for future development. Ongoing work aims to define molecular target engagement and refine mechanistic understanding to guide next-generation design.

molecular biology↗

Fever-range temperature enhances B cells in vitro but is dispensable for the germinal center in vivo

Fever is a conserved physiological response to immune activation characterized by elevated body temperature. While hyperthermia enhances innate and T cell immunity, its role in shaping the B cell compartment remains poorly defined, despite B cells' role in long-term protection. Understanding how temperature modulates B cell physiology is relevant to vaccine strategies, particularly fever management around immunization. Therefore, we investigated the influence of fever-range thermal changes on humoral immunity. To decipher the direct effects, primary B cells from C57BL/6 mice were stimulated in vitro under mild hyperthermic conditions (~1.5{degrees}C increase). Fever-range temperature enhanced B cell activation, facilitated entry into cell division, and increased antigen presentation to CD4+ T cells, while transcriptomic analysis revealed enrichment of pathways involved in protein synthesis and mitochondrial respiration. To determine whether these intrinsic effects translated into altered humoral immunity in vivo, we developed a novel tunable implant-based system to induce localized, 48-hour hyperthermia around a draining lymph node in awake mice without altering core body temperature. Following subcutaneous NP-OVA/alum immunization, localized hyperthermia localized hyperthermia did not enhance antigen-specific germinal center B cell expansion, antibody titers or IgG affinity on day 9. Moreover, heating during priming did not affect the recall humoral response after a booster on day 21. Thus, fever-range temperature directly modulates murine B cell function in vitro but does not enhance humoral immunity in vivo, indicating that the biological consequences of intrinsic B cell thermosensitivity depend on its integration within the multicellular and inflammatory signals shaping germinal center responses.

immunology↗

Stimulatrix: An open-source automated platform for high-throughput functional characterization of engineered contractile tissues

Engineered cardiac and skeletal muscle tissues suspended between flexible posts support disease modeling and pharmacology, yet their stimulation, longitudinal imaging and quantitative analysis often remain fragmented and labor-intensive. Here we present Stimulatrix, an open-source platform integrating automated video acquisition within a cell culture incubator, synchronized electrical stimulation and deep learning for longitudinal assessment of contractile tissues in multiwell plates. The platform quantifies tissue compaction, force generation and contraction kinetics with optional cloud processing reducing dependence on local GPU hardware. We demonstrate the workflow in cardiac tissues comprising human induced pluripotent stem cell-derived cardiomyocytes and cardiac fibroblasts, and in primary human skeletal muscle constructs. Force and kinetic measurements were benchmarked against manual annotations. Longitudinal profiling resolved responses to matrix composition and pacing regimens and tracked doxorubicin-associated loss of cardiac contractile force. Stimulatrix provides an accessible workflow for automated functional phenotyping of engineered muscle tissues.

bioengineering↗

PMBB Geno-Pheno Toolkit: A suite of scalable, reproducible pipelines for cross-biobank association analyses

SummaryElectronic health record (EHR)-linked biobanks generate unprecedented genomic and phenotypic datasets, but their scientific utility is constrained by data fragmentation across institutional silos and incompatible computing infrastructures, forcing researchers to rewrite ad-hoc scripts for each new environment. We present the PMBB Geno-Pheno Toolkit, a suite of modular Nextflow pipelines for biobank-scale association analyses. This note focuses on the toolkits SAIGE family of pipelines -- supporting genome-wide (GWAS), exome-wide (ExWAS), and phenome-wide (PheWAS) association testing -- together with the companion GWAMA and ExWAS meta-analysis pipelines that enable cross-biobank replication. All components are containerized (Docker/Apptainer) and orchestrated with Nextflow, allowing the same workflows to run unmodified on local HPC clusters, cloud platforms, and the All of Us Research Workbench. Complementary toolkit pipelines for PLINK-based GWAS, polygenic scoring, LD-based clumping, and phenotype harmonization are also available and briefly noted. AvailabilityThe PMBB Geno-Pheno Toolkit is freely available at https://github.com/PMBB-Informatics-and-Genomics/pmbb-geno-pheno-toolkit under MIT open-source license.

bioinformatics↗

High spatial resolution 23Na-MRI for ischemic brain injury detection

High spatial resolution sodium (23Na) imaging of brain lesions remains challenging due to the intrinsically low signal-to-noise ratio (SNR) of 23Na-MRI compared with conventional proton (1H) MRI. In this study, we established a high-resolution 23Na-MRI platform based on 14 T preclinical scanner using a dual-tuned head-implanted RF coil. This configuration enables the acquisition of 1H-based T2-weighted anatomical and diffusion-weighted imaging (DWI), as well as 23Na-MRI, from the same animal. Brain-wide 23Na-MRI with 300x300 {micro}m2 in-plane resolution was performed within the first 4 hours after acute middle cerebral artery occlusion (MCAO) induced ischemic stroke induction. Hyperintense 23Na-MRI signals were observed in the ischemic brain regions, presenting a contrast-to-noise ratio (CNR) that exceeded that of T2-weighted images. Infarct regions can be well-identified in the elevated 23Na signal, which is spatially consistent with regions of reduced apparent diffusion coefficient (ADC) values, indicating water restriction in the ischemic core. This work established implanted double-tuned 1H/23Na RF coils as a powerful approach for high-resolution 23Na-MRI readout, facilitating the early detection of ischemic brain injury.

neuroscience↗

Viral Infections Drive Functional Remodeling of Ribosome-Associated Proteins

Viruses hijack host ribosomes to synthesize their proteins and have evolved various strategies to manipulate translation, including the association of numerous non-ribosomal proteins, known as ribosome-associated proteins (RAPs), with the core ribosome. However, current methods of capturing RAPs that associate transiently and/or in small amounts with ribosomes are suboptimal. To address this issue, we developed an enhanced ribosome affinity purification (eRAP) method that enables the capture of over 500 previously unreported RAPs. Using eRAP, we investigated whether the composition of ribosomes changes during infection by two very different viruses: herpes simplex virus 1 (HSV-1) and Sindbis virus (SINV). Our results revealed that viral infection does not substantially alter the composition of core ribosomes but does drive extensive remodeling of RAPs in a virus-specific manner. Functional analyses with SINV showed that several of these RAPs are critical for viral propagation. Additionally, we discovered that the RAP ASCC3 plays a novel role in promoting the expression of secretory proteins, including viral glycoproteins. This occurs independently of ASCC3s canonical function of rescuing ribosome collisions. Together, our findings establish the ribosome as a dynamic regulatory hub that undergoes remodeling to achieve virus-specific translational output, highlighting the functional significance of ribosomal heterogeneity.

molecular biology↗

Evaluating the performance of photon- and electron-based fragmentation methods in Omnitrap-LCMS analysis of N-glycopeptides

To date, collision-induced dissociation and methods based on electron transfer dissociation are considered the standard approaches for the mass spectrometry analysis of N- and O-glycopeptides, respectively, allowing for identification of both peptide and glycan compositions. In recent years, alternative fragmentation methods such as ultraviolet photodissociation (UVPD) and more energetic versions of electron-based techniques (such as electron ionisation dissociation, EID) have been shown to be useful for the analysis of glycopeptides, producing rich information on the glycopeptide structure, including types of glycosidic linkages. We evaluated ultraviolet photodissociation (UVPD), electron ionization dissociation (EID), electron capture dissociation (ECD), and activated-ion ECD (AI-ECD) using an Orbitrap-Omnitrap hybrid for LC-MS analysis of complex N-glycopeptides. Both UVPD and EID generated extensive peptide, glycosidic, and cross-ring fragments, enabling detailed structural characterization. While ECD alone produced few glycopeptide identifications, AI-ECD significantly improved yields through supplemental vibrational activation. UVPD and EID achieved comparable identification efficiencies to stepped collisional dissociation and provided additional linkage information. These results establish the Omnitrap as a powerful platform for comprehensive glycoproteomic analysis and highlight the need for enhanced computational tools to interpret complex UVPD and EID spectra.

systems biology↗

Hepatocyte MLKL Drives Obesity-Driven Hepatocellular Carcinoma Progression via Mitochondrial Dysfunction Independent of Necroptosis in MASLD

Background and AimsMetabolic dysfunction-associated steatotic liver disease (MASLD) is a leading cause of hepatocellular carcinoma (HCC), particularly in obesity, yet mechanisms linking hepatocyte dysfunction to tumorigenesis remain unclear. Mixed lineage kinase domain-like protein (MLKL), the effector of necroptosis, is elevated in MASLD, but its hepatocyte-intrinsic role in obesity-driven MASLD-HCC is unknown. Approach and ResultsUsing a long-term Western diet (WD)-induced MASLD-HCC model in hepatocyte-specific MLKL knockout (MlklHepKO) mice, we defined MLKLs hepatocyte-intrinsic function. WD increased hepatocyte MLKL protein expression without detectable necroptosis activation, indicating a necroptosis-independent role. MLKL deficiency did not alter WD-induced inflammation, fibrosis, or liver injury but increased hepatic lipid accumulation while reducing lipotoxic lipid species and preserving mitochondrial function. WD-fed MlklHepKO mice developed fewer and smaller tumors with reduced incidence, multiplicity, proliferation, and stemness. Transcriptomic analysis revealed upregulation of mitochondrial oxidative phosphorylation pathways in MlklHepKO livers. WD suppressed the mitochondrial fusion protein and tumor suppressor MFN2, whereas MLKL deficiency restored MFN2 expression post-translationally. In HCC cells, MLKL deletion reduced proliferation, improved mitochondrial respiration, and decreased glycolysis; these effects were reversed by MFN2 deletion. MLKL localized to nuclear and mitochondrial compartments, consistent with organelle-intrinsic functions. The human MLKL inhibitor necrosulfonamide (NSA) suppressed HepG2 xenograft growth, and elevated MLKL expression in human HCC correlated with poorer overall survival. ConclusionsHepatocyte MLKL promotes MASLD-associated HCC through a non-necroptotic mechanism involving MFN2 suppression, impaired mitochondrial function, and increased tumor proliferation and stemness. These findings identify MLKL as a potential therapeutic target in MASLD-associated HCC.

cancer biology↗

High-throughput discovery of a dearomative cycloaddition enables dual photochemical-photophysical perturbative probing of protein function

Proteins exist in multiple conformations or states, often associated with different functional capacities. The ability to selectively identify and study these states is crucial for understanding the dynamic nature of proteins and their roles in cellular processes, yet can be currently limited by the artefacts of existing molecular labels and the lack of strategies to exploit them in diverse ways. Whilst i) methods for the photochemical perturbation of proteins and ii) photophysical protein probes and sensors are both known powerful tools, simultaneous methods for site- and context-specific photochemical modification of a protein side chain with concomitant modulation of photophysical properties would allow interrogation of protein function via diverse modes (potentially reporting simultaneously on structure and dynamics of ground- and reactive-state properties). Due to their mechanistic complexity, rational approaches for the design of suitable photochemical strategies can be difficult and non-intuitive. Here, we describe a high-throughput experimentation (HTE) strategy designed to allow the photochemical modification of a genetically-encoded, minimally disruptive ( zero-size), photophysically-active - yet typically unreactive and biologically-inert - unnatural amino acid (uAA) residue in proteins. The discovery of a novel dearomative, formal [4+3] photocycloaddition of imidazopyrimidine reagents which proceeds via photochemically generated C* intermediates with polyaromatic substrates enabled chemoselective application to the normally unreactive Trp-mimetic residue, 2-naphthylalanine (Npa). Npas site-selective installation allows dual photochemical and photophysical dearomative perturbation benignly and efficiently in proteins. Replacement of Trp in the archetypal apoptotic biosensor protein Annexin A5 (AnxV) enabled dual photochemical-photophysical determination of switched, conformationally-determined reactive states induced by Ca2+-binding, without any apparent functional perturbation of its in vitro or cellular recognition of phospholipids, indicating an ordered annexin mechanism. This ready and benign unification of photochemistry and photophysics suggests a general approach for using high-throughput light-mediated experimentation in artefact-free chemical biology to capture different functional states of proteins and to interrogate those states using combined photochemical-photophysical methods. HighlightsO_LIDevelopment of a general, high-throughput experimentation (HTE) approach enabled identification of an unprecedented photochemical reaction with potential for editing amino acid side chains within proteins. C_LIO_LIGenetic incorporation of 2-naphthylalanine, a minimally-disruptive ( zero-size) Trp mimic, enabled photochemical side chain editing with concomitant modulation of its distinctive photophysical properties in proteins. C_LIO_LIA naphthalene-tagged variant of the apoptotic biomarker protein AnxV enabled dual photochemical-photophysical exploration of its dynamic conformational states induced by Ca2+-binding whilst fully maintaining its functional capacity for in vitro or cellular recognition of phospholipids. C_LI

biochemistry↗

Biomolecular tracking by FIRESCAPE reveals distinct modes of clearance, damage induction and cellular uptake for extracellular histone H3

In attempting to observe the behaviour of a protein of interest in vivo, akin to other observer effects, current techniques require modifications or interventions that inherently alter the protein or its host, leaving one uncertain as to whether natural behaviour remains unperturbed. The study of chromatin has mostly been restricted to defining its function in the nucleus, where histone proteins fulfil vital roles in packaging genomic DNA and regulating transcription. However, chromatin components can be released into the extracellular space, either intentionally via cellular secretion or during disease-induced cell death. These extracellular chromatin components, depending on the context, can consist of: free histones, free DNA, intact nucleosomes (histone octamers wrapped by DNA), or heterogeneous, higher order structures such as neutrophil extracellular traps (NETs). They have been associated with diverse pathologies such as inflammation, cancer, and sepsis, and distinct toxic effects. However, there is a widely acknowledged lack of methods that distinguish between them and between their unique functions. Here, we now address protein observer effects to explore the fate and function of extracellular free histones by utilizing FIRESCAPE ([18F]-Fluorine Isotopic Radiolabeling Enabling Scanning of Clearance After Proteolytic Events), a novel radiolabeling concept that leverages the unique, high-sensitivity properties of the radioisotope fluorine-18, 18F, and residue-specific protein editing chemistry. By installing close and then true 18F-containing protein sidechain mimics site-specifically, FIRESCAPE enables the hierarchical in vivo scanning of the half-lives, proteolytic susceptibility and clearance of single residues in a protein of interest, and at microdoses far below toxic levels (low nanomole). These radioequivalent proteins bearing near-zero-size, zero-background labels now precisely reveal the strikingly distinct distribution, half-lives, damage-inducing abilities and accumulation of free extracellular histones in cellulo and in vivo compared to intact nucleosomes. Free extracellular histone H3 is rapidly cleared from circulation, mediated first by proteolysis of the histone tail. By contrast, direct injection of free histones vs nucleosomes into tissue that is unprotected by such proteolysis (brain), provokes a starkly different response; free histones exhibited limited diffusion and swiftly promoted damage both in cell culture and in vivo, whilst intact nucleosomes were essentially passive and benign. Remarkably, synthetic extracellular histone H3 was observed to enter cells and integrate into chromatin, indistinguishable from native H3 in both localization and post-translational modification (PTM) accumulation, yet paired with cellular and tissue damage. The exploratory studies described here now provide much needed clarity to the distinct fates and effects of extracellular histones vs nucleosomes, in particular the strongly damaging effects of free histones, their rapid uptake into cells, and an associated histone-specific proteolysis pathway via the removal of the histone tail.

biochemistry↗

Discovery of Niclosamide Analogs with Potent Mitochondrial Uncoupling Activity with reduced toxicity

Mitochondrial uncouplers have shown clinical potential across various diseases, including cancer. Niclosamide, an FDA-approved anthelmintic drug, acts as a mild mitochondrial uncoupler and has demonstrated anticancer activity in multiple preclinical cancer models. However, its clinical application remains limited, with some attributing this to poor bioavailability, while the underlying mechanisms are still unclear. Here, we demonstrate that niclosamide exhibits a dose-dependent biphasic effect, promoting uncoupling at low concentration while acting as a mitochondrial inhibitor at high concentration, which could restrict its therapeutic window and limit efficacy. To overcome this challenge, we aimed to develop next-generation mitochondrial uncouplers (MUs) by synthesizing and evaluating novel Niclosamide derivatives with enhanced therapeutic potential. Through structural modifications, we optimized uncoupling activity while reducing inhibitory toxicity, thereby expanding the pharmacological window. Our findings suggest that fine-tuning the molecular structure of mitochondrial uncouplers could provide a safer and more effective metabolic reprogramming strategy for cancer treatment.

pharmacology and toxicology↗

Integrating Alternative Fragmentation Techniques into Standard LC-MS Workflows Using a Single Deep Learning Model Enhances Proteome Coverage

We built and characterised a mass spectrometer capable of performing CID (both beam type and resonant type), UVPD, EID and ECD in an automated fashion during an LCMS type experiment. We exploited this ability to generate large datasets through multienzyme deep proteomics experiments for characterisation of these activation techniques. As a further step, motivated by the complexity generated by these dissociation techniques, we developed a single Prosit deep learning model for fragment ion intensity prediction covering all of these techniques. The generated model has been made publicly available and has been utilised in FragPipe within its MSBooster module. Rescoring allowed both data-dependent acquisition (DDA) and data-independent acquisition (DIA) to achieve on average more than 10% increase in protein identifications across all dissociation techniques and enzymatic digestions. We demonstrate that these alternative fragmentation approaches can now be used within standard data analysis pipelines and can produce data competitive to CID in terms of eficiency, but in the cases of EID and UVPD with far richer and more comprehensive spectra.

systems biology↗

RNA binding regulation is a new dimension in the type I IFN response

The type I interferon (IFN-I) response shapes the intracellular environment to supress virus infection. Historically, this remodelling has been linked to the transcriptional induction of interferon stimulated genes (ISGs). However, IFN-I-driven post-translational regulation of proteins already present in the cell remains relatively unexplored. Here, we profiled the activity of cellular RNA-binding proteins (RBPs), which are key players in antiviral immunity. Using RNA interactome capture (RIC), we identified hundreds of RBPs whose association with RNA is regulated by IFN-I (IR-RBPs). Among these IR-RBPs are both known antiviral proteins and novel candidates identified in this study through a knockdown screen. By modifying RIC to study IR-RBPs phosphorylation states, we identified several putative instances of IFN-I-driven phospho-regulation of RNA binding. We experimentally confirmed this phospho-driven regulation for MATR3. Altogether, our results reveal a new dimension of the cells antiviral programme, in which the cellular RNA-bound proteome is remodelled by IFN-I.

biochemistry↗

Are Solid Particles Ready for Prime-Time Proteomics?

We evaluate the performance of nonporous C-18 stationary phases in high-speed proteomics workflows. We employed two commercially available sub-2 {micro}m nonporous particle (NPP) materials, ODS-IIIE (1.5 {micro}m) and SOLAD (1.0 {micro}m), to fabricate analytical columns using 150 {micro}m internal diameter (i.d.) fused silica capillaries to ensure compatibility with nano-UHPLC and nano-HPLC pressure regimes. Using long NPP columns (15 - 25 cm) connected to a conventional nano-UHPLC, we found that both materials supported efficient peptide separations within the flow rate and pressure ranges typical of nano-UHPLC systems. Shorter columns, used with the 10- and 16-minute Whisper Zoom 120 and Zoom 80 methods on the Evosep One HPLC, demonstrated competitive separation performance compared to columns packed with fully porous (FPP) and superficially porous particles (SPP), achieving full-width at half maximum (FWHM) values below 2 seconds (Zoom 120) and 3 seconds (Zoom 80). DIA LC-MS/MS analysis of the same digest demonstrated that NPP columns provided comparable or superior performance relative to FPP and SPP materials. These findings establish NPP-based columns as a viable and competitive alternative to FPP and SPP materials, particularly suited for high-throughput and high-sensitivity proteomics applications.

systems biology↗

A Non-canonical Role for Hepatocyte MLKL in Promoting Mitochondrial Dysfunction and Senescence in the Aging Liver

Liver aging is characterized by chronic inflammation and metabolic dysfunction that contributes to the progression of metabolic dysfunction-associated steatotic liver disease (MASLD). Necroptosis, a form of inflammatory cell death, is activated in aging livers, and genetic (Ripk3-/-or Mlkl-/- mice) or pharmacological (RIPK1 inhibitor necrostatin-1s) inhibition of necroptosis attenuates liver inflammation and pathology. However, the cell type-specific role of necroptosis in liver aging remains unclear. Given that MLKL is expressed in hepatocytes, and its expression increases with age, we generated hepatocyte-specific MLKL-overexpressing mice (MLKLHepOE) to determine its role in liver aging. Unexpectedly, MLKL overexpression in hepatocytes did not induce necroptosis, but instead upregulated markers of cellular senescence (cell cycle arrest genes and SASP factors), increased macrophage infiltration, and elevated M1 macrophage marker expression. Electron microscopy and mitochondrial analyses revealed abnormal mitochondrial morphology, elevated oxidative stress, and disrupted mitochondrial dynamics, while lipidomics demonstrated alterations in hepatic lipid metabolites. In agreement with our observations in MLKLHepOE mice, MLKL overexpression in AML12 hepatocytes impaired mitochondrial respiration, increased proinflammatory extracellular vesicle (EV) release, and induced senescence markers, without triggering cell death. Together, these findings reveal a non-lethal, non-necroptotic role for MLKL in promoting hepatocyte senescence and metabolic dysfunction via mitochondrial impairment and EV-mediated inflammation. Our study highlights MLKL as a novel driver of liver inflammaging and a potential therapeutic target for age-related liver disease.

cell biology↗

Efficient packaging of HIV-1 genomes via recognition of its adenosine-rich content by a heterologous RNA-binding domain

The HIV-1 genome (gRNA) has an unusually biased nucleotide content and is rich in adenosines. Selective packaging of the gRNA is thought to be driven by specific binding of the nucleocapsid (NC) domain of the viral Gag protein to the packaging signal ({Psi}) in the host cell cytosol. However, deletion of regions within {Psi} reduces--but does not completely abolish--genome packaging. To probe whether another feature of the gRNA may contribute to the selective gRNA packaging process, we replaced NC with heterologous RNA-binding domains (RBDs) with distinct RNA-binding properties. Surprisingly, despite disparate RNA binding specificities, all Gag-RBD chimeras successfully recruited the gRNA to the plasma membrane, suggesting that the initial gRNA recognition in the cytosol is not rate limiting. Notwithstanding, many chimeras exhibiting G/C binding specificity were arrested at the assembly stage. Only the Gag-SRSF5 chimera, which multimerized efficiently on adenosine-rich sequences on the gRNA, assembled efficiently and packaged gRNA at near wild-type levels. Importantly, rationally designed mutations that altered the A/G-rich binding specificity of Gag-SRSF5 decreased genome encapsidation efficiency. Furthermore, many Gag chimeras displayed potent dominant negative activities, highlighting NC functions as a targetable step in virus replication. Together, our findings reveal an unexpected aspect of the HIV-1 gRNA, its biased nucleotide content, as a key driver of selective genome packaging. SIGNIFICANCEHow HIV-1 selectively packages its genome (gRNA) into virions is poorly understood. To probe this, we replaced the viral nucleocapsid (NC) protein with heterologous RNA-binding domains (RBDs) from cellular hnRNP and SR protein families. Remarkably, despite their distinct RNA-binding specificities, all Gag-RBD chimeras successfully recruited the gRNA to the plasma membrane, suggesting that the initial gRNA recognition is not rate limiting. Only the Gag-SRSF5 chimera packaged gRNA efficiently which correlated with its capacity to multimerize on adenosine-rich sequences on the gRNA. Notably, several Gag chimeras exhibited strong dominant negative effects, underscoring NC functions as a targetable step in virus replication. Together, these findings uncover that the biased nucleotide content of the HIV-1 gRNA facilitates its selective packaging into virus particles.

microbiology↗

A Critical Role for Neutral Sphingomyelinase-2 in Doxorubicin-induced Cardiotoxicity

Cardiotoxicity is a major side effect of Doxorubicin (Dox) that has hampered its clinical utility, and strategies to mitigate this cardiotoxicity are limited. Sphingolipids (SL) are central to the chemotherapy response in cancer but their role in normal tissue is less clear. Here, we identified the SL enzyme neutral sphingomyelinase-2 (nSMase2) as a critical mediator of chronic Dox-induced cardiotoxicity, establishing nSMase2 as a key downstream effector of Dox in cardiomyocytes (CM) and showing that in vivo loss of nSMase2 activity is protecting against chronic Dox-induced cardiac damage and dysfunction. Biologically, these studies link nSMase2 with Dox-induced CM senescence both in vitro and in vivo and identify the dual specificity phosphatase DUSP4 as a novel effector of nSMase2 in the Dox response. In addition to cementing a role for SL metabolism in Dox effects in normal tissue, this study advances nSMase2 as a target of interest for cardioprotection.

cell biology↗