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Hammond, C.

Publications and source records attributed to Hammond, C..

13 recordsLinked to original sources

Evaluating Spike Antigenicity across Endemic Human Coronavirus Models using Flow Virometry

While SARS-CoV-2 research has advanced rapidly since COVID-19, endemic human coronaviruses (HCoVs) remain comparatively understudied. Tools to phenotype spike (S), the primary antigenic target on coronaviruses, at the single-virion level could improve vaccine design by capturing variation in epitope availability and spike abundance. Here, we establish a calibrated flow virometry (FV) platform to quantify S antigenicity on native endemic (HCoV-229E, HCoV-OC43) and epidemic (SARS-CoV-2) coronaviruses directly in cell culture supernatants. FV revealed cell line-dependent differences in S antigenicity, including receptor-induced changes in epitope accessibility. Comparison of virion-associated S with recombinant stabilized S by ELISA and biolayer interferometry showed consistent binding for HCoV-OC43, MERS-CoV, and SARS-CoV-2, but differences for HCoV-229E, with FV resolving heterogeneity not captured by bulk assays. Finally, FV showed that HCoV-229E from patient-derived air-liquid interface cultures exhibited reduced antibody binding and distinct S antigenicity compared to cell line-derived virions. Together, these findings establish FV as a platform for single-virion analysis of HCoV antigenicity.

microbiology↗

Evaluating the Utility of a Nanoscale Flow Cytometer for Detection of Surface Proteins on HIV and Extracellular Vesicles

BackgroundFlow virometry (FV) - the application of flow cytometry to viruses - has historically been hindered by the inability of cytometers to detect particles below [~]300 nm in size. However, advances in optics and fluidics have enabled cytometers primarily designed for cells to detect viruses and extracellular vesicles (EVs) through light scatter alone. In 2024, the CytoFLEX nano was released, marketed for the detection of particles as small as 40 nm; however, its performance has yet to be compared to a conventional instrument for FV. MethodsFV was utilized to evaluate performance of the CytoFLEX nano and a conventional flow cytometer (CytoFLEX S). Instrument scatter sensitivity was assessed using NIST beads (40-400 nm), and virus stocks [human immunodeficiency virus (HIV), human coronaviruses (HCoV)-229E and HCoV-OC43]. For fluorescence analysis, HIV virions were stained with PE- and BV421-conjugated antibodies targeting virion incorporated proteins (CD38, CD44), individually and in combination. Finally, HIV stocks were labeled with antibodies against the envelope (Env) glycoprotein and tetraspanins (CD9, CD81) to assess EVs within virus preparations. ResultsCompared to the CytoFLEX S, the CytoFLEX nano exhibited substantially greater scatter sensitivity, reflected by up to 50-fold higher signal-to-noise ratio across NIST-traceable beads and virus samples. This enabled clearer resolution of smaller populations, including bead populations < 70 nm that were undetectable on the CytoFLEX S, as well as improved resolution across all viruses. While both instruments reliably detected stained proteins on HIV virions, the CytoFLEX nano revealed a distinct population of tetraspanin-positive EVs within HIV stocks that was undetected on the CytoFLEX S. Using GFP-tagged HIV, we identified Env+ particles lacking GFP, indicating the presence of Env on EVs. ConclusionsThe CytoFLEX nano exhibited markedly improved scatter sensitivity compared to the CytoFLEX S, improving detection of viruses and enabling detection of EV populations that were undetectable on the conventional instrument. While both platforms performed similarly for surface protein labeling, additional consideration of spectral overlap was needed with the CytoFLEX nano in multicolor experiments. These findings highlight that the complementary strengths of each platform can be utilized to more comprehensively characterize virus and EV populations, providing new opportunities to investigate nanoparticle heterogeneity.

microbiology↗

Trump Administration Impacts on Early Career Scientists and How To Fight Back

Scientific research drives national progress and innovation, and must be protected at all costs. Actions from the Trump administration in early 2025 sent shockwaves across academic research. Federal science budgets were slashed, hundreds of research grants were abruptly frozen or terminated, and politically appointed agency heads overrode peer-reviewed grant decisions. We conducted rapid-response surveys to capture quotes, stories, and data to understand how these seismic shifts were being felt by early career researchers. The majority of survey respondents were PhD students, and early career trainees in varying years of training at a variety of institutions, mainly in the life sciences. Their future in research, funded by major science agencies including NIH, was threatened by funding cuts with varying impacts to their professional endeavors. Survey respondents highlighted concerns with long-term research job prospects and broader systemic issues in academia, leading them to consider leaving the field altogether and/or pursue science in another country. Their opinions highlighted concerns at the undergraduate, graduate, and postdoctoral levels. While universities provided some resources, trainees called upon Congress to protect, stabilize, and restore science funding. They also undertook a number of advocacy actions across the nation. The fight is far from over. Continued support for early career researchers and their careers in research is imperative to continue both in the current environment and into the future, in order to develop a strong workforce and ensure U.S. global competitiveness in science and technology fields.

scientific communication and education↗

Human Coronavirus HKU1 Neutralizing Monoclonal Antibodies Target Diverse Epitopes Within and Around the TMPRSS2 Receptor Binding Site

Endemic human coronaviruses (HCoVs), such as HCoV-HKU1, account for [~]30% of common colds each year and can cause serious upper and lower respiratory infections, yet no licensed vaccines or therapeutic antibodies target HCoVs. Despite being endemic to the human population, little is known about the antigenic landscape of HCoV-HKU1. Here, we characterized key interactions between the HCoV-HKU1 spike (S) protein and monoclonal antibodies (mAbs) isolated from convalescent HCoV-HKU-1-positive peripheral blood mononuclear cells collected prior to the COVID-19 pandemic. We isolated 14 mAbs that bound distinct regions of S, including the receptor-binding domain (RBD), N-terminal domain, and S2 subunit. Structural and functional studies revealed three groups of RBD-specific mAbs targeting diverse footprints within and around the TMPRSS2 receptor-binding site: (1) H501-022, which recognizes the TMPRSS2-binding site and thereby blocks receptor engagement; (2) H501-008, which binds a distinct epitope outside the TMPRSS2-binding site that is shared with HCoV-OC43; and (3) H501-018, which recognizes both "up" and "down" RBD conformations at a distinct, non-overlapping epitope outside the TMPRSS2-binding site. H501-008 weakly neutralized live HCoV-OC43 in vitro and protected mice against lethal HCoV-OC43 challenge. Notably, the three RBD-specific mAbs potently neutralized HCoV-HKU1 pseudovirus in TMPRSS2-overexpressing cell lines, but exhibited limited neutralizing activity against authentic HCoV-HKU1 infection in primary human airway epithelial cells. Together, these findings structurally define the antigenic landscape within and around the HKU1 receptor-binding site and demonstrate that receptor-binding site recognition alone is insufficient to predict physiologically relevant antibody-mediated neutralization.

microbiology↗

Projection Targeting with Phototagging to Study the Structure and Function of Retinal Ganglion Cells

Visual information from the retina is sent to diverse targets throughout the brain by different retinal ganglion cells (RGCs). Much of our knowledge about the different RGC types and how they are routed to these brain targets is based on mice, largely due to the extensive library of genetically modified mouse lines. To alleviate the need for using genetically modified animal models for studying retinal projections, we developed a high-throughput approach called projection targeting with phototagging that combines retrograde viral labeling, optogenetic identification, functional characterization using multi-electrode arrays, and morphological analysis. This method enables the simultaneous investigation of projections, physiology, and structure-function relationships across dozens to hundreds of cells in a single experiment. We validated this method in rats by targeting RGCs projecting to the superior colliculus, revealing multiple functionally defined cell types that align with prior studies in mice. By integrating established techniques into a scalable workflow, this framework enables comparative investigations of visual circuits across species, expanding beyond genetically tractable models. MotivationVisual information from the retina is distributed to diverse targets throughout the brain. Much of our knowledge about how visual information is processed and routed to these brain targets is based on mice because of the large library of genetically modified mouse lines. For most other species, such libraries are not available. Therefore, we were motivated to develop an approach for characterizing diverse retinal projections into the brain that can be applied to other species. We aimed to achieve projection targeting with retrograde viral vectors, followed by identification of circuit-specific retinal ganglion cells (RGCs) with optogenetics, functional characterization with multi-electrode array (MEA) recordings, and morphological description with in situ and confocal microscopy. The resulting high-throughput approach permits functional and morphological investigation of dozens to hundreds of cells in individual experiments. By replacing the need for genetically modified animals with a suite of standard techniques, this approach should improve cross-species comparisons of the initial stages of visual processing. SummaryUnderstanding the structure-function relationships across neurons is challenging, particularly when circuits are composed of dozens of distinct cell types. We refined an approach, called projection targeting with phototagging, that allows simultaneous elucidation of the projections, morphology, and visual response properties of diverse RGC types in the mammalian retina. The approach combines retrograde virally mediated phototagging of RGCs, microscopy, and large-scale MEA measurements. Importantly, the approach does not rely on transgenic animals and thus is generalizable across species. We validated this approach in rats by targeting retinal projections to the superior colliculus (SC). We showed that multiple RGC types project to the SC and that these results in rats align well with prior findings from transgenic mouse studies. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=194 HEIGHT=200 SRC="FIGDIR/small/661576v1_ufig1.gif" ALT="Figure 1"> View larger version (49K): org.highwire.dtl.DTLVardef@1003310org.highwire.dtl.DTLVardef@1881cdorg.highwire.dtl.DTLVardef@f1dba1org.highwire.dtl.DTLVardef@8a539f_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIThe viral vector, AAV2retro, is effective for delivering opsins to retinal ganglion cells (RGCs) for phototagging and projection mapping. C_LIO_LIPhototagging allows matching RGC visual responses to morphology, while also identifying their central projections. C_LIO_LIThe approach does not rely on genetically modified animals and thus is generalizable across species. C_LI

neuroscience↗

Schwann cells modified to secrete MANF is a potential cellular therapy for peripheral nerve regeneration

Despite several decades of research, an effective therapy for peripheral nerve regeneration is still lacking. The lack of knowledge of molecular candidates that equally promote axon regeneration and glial cell dynamics essential for regeneration poses challenges in developing effective therapies. Improper optimization of potential therapies leading to failures in ensuring their local availability in nerves also poses additional challenges. Here, we showed that the neurotrophic factor, the mesencephalic astrocyte-derived neurotrophic factor (MANF), equally promotes axon regeneration and glial cell dynamics favorable for nerve regeneration. We showed that while endogenous expression of MANF is primarily restricted to non-peptidergic sensory neurons in adult rats, exogenous MANF promotes the growth of all subtypes of adult rat sensory neurons. We also demonstrated that exogenous MANF promotes the proliferation and migration of adult rat primary Schwann Cells (SCs). Further, we found that local and repeated administration of exogenous MANF to injured mouse nerve promote axon regeneration. Finally, we devised a therapeutic approach by programming nerve resident SCs to locally and continuously deliver MANF to injured rat nerves and showed that this approach improved nerve regeneration indices. Overall, this work developed a therapeutic approach by harnessing the power of SCs as a local delivery system of MANF for improving nerve regeneration.

neuroscience↗

Human lymphoid-neutrophil/monocyte restriction co-ordinately activates increased proliferation despite parallel heterogeneity in transcriptional changes

Recent studies indicate the human lympho-myeloid restriction process to be a different and more heterogeneous one than historically inferred. Here we describe the development of bulk and clonal culture systems that efficiently support early B-lymphoid differentiation and their use to identify biological and molecular changes that accompany their initial restriction from subsets of CD34+ human cord blood cells with lympho-myeloid-limited potential. Analyses of the changes observed revealed the acquisition of B-lymphoid- and neutrophil/monocyte (NM)-restricted properties are accompanied by a concomitantly accelerated and lineage-shared cell cycling activity and loss of self-renewal properties. Parallel, single-cell transcriptome analysis identified reduced expression of multiple self-renewal-associated genes and an accompanying heterogeneous activation of lineage-regulatory modules during the production of B, NM and dendritic cell precursors. These results uncover a connected regulation of lineage-shared proliferation control with persistent heterogeneity in the biological and transcriptional changes in the same cells undergoing B and NM lineage restriction.

immunology↗

Polycomb contraction differentially regulates terminal human hematopoietic differentiation programs

Lifelong production of the many types of mature blood cells from less differentiated progenitors is a hierarchically ordered process that spans multiple cell divisions. The nature and timing of the molecular events required to integrate the environmental signals, transcription factor activity, epigenetic modifications, and changes in gene expression involved are thus complex and still poorly understood. We now show that the more primitive types of human cells in this system display a unique repressive H3K27me3 signature that is retained by mature lymphoid cells but is lost in terminally differentiated monocytes and erythroblasts. Additional intervention data implicate that control of this chromatin state change is a requisite part of the process, whereby normal human hematopoietic progenitor cells make lymphoid and myeloid fate decisions.

cell biology↗

A rare SMAD9 mutation identifies the BMP signalling pathway as a potential osteoanabolic target

To identify targets for novel anabolic medicines for osteoporosis, we recruited a large cohort with unexplained high bone mass (HBM). Exome sequencing identified a rare (minor allele frequency 0.0014) missense mutation in SMAD9 (c.65T>C, p.Leu22Pro) segregating with HBM in an autosomal dominant family. The same mutation was identified in another two unrelated individuals with HBM. In-silico protein modelling predicts the mutation severely disrupts the MH1 DNA-binding domain of SMAD9. Affected individuals have bone mineral density [BMD] Z-Scores +3 to +5, with increased volumetric cortical and trabecular BMD, increased cortical thickness, and low/normal bone turnover. Fractures and nerve compressions are not seen. Both genome-wide, and gene-based association testing of heel estimated-BMD in >362,924 UK-Biobank British subjects showed strong associations with SMAD9 (PGWAS=6x10-16; PGENE =8x10-17). Smad9 is highly expressed in murine osteocytes and zebrafish bone tissue. Our findings support SMAD9 as a novel HBM gene, and a potential novel osteoanabolic target.

genetics↗

Variable Retention of Differentiation-specific DNA Replication Timing in Human Pediatric Leukemia

Human B-lineage precursor acute lymphoid leukemias (BCP-ALLs) comprise a group of genetically and clinically distinct disease entities with features of differentiation arrest at known stages of normal B-lineage differentiation. We previously showed BCP-ALL cells display unique and clonally heritable DNA-replication timing (RT) programs; i.e., programs describing the variable order of replication of megabase-scale chromosomal units of DNA in different cell types. To determine the extent to which BCP-ALL RT programs mirror or deviate from specific stages of normal human B-cell differentiation, we transplanted immunodeficient mice with quiescent normal human CD34+ cord blood cells and obtained RT signatures of the regenerating B-lineage populations. We then compared these with RT signatures for leukemic cells from a large cohort of BCP-ALL patients. The results identify BCP-ALL subtype-specific features that resemble specific stages of B-cell differentiation and features that appear associated with relapse. These results suggest the genesis of BCP-ALL involves alterations in RT that reflect clinically relevant leukemia-specific genetic and/or epigenetic changes. SUMMARYGenome-wide DNA replication timing profiles of >100 pediatric leukemic samples and normally differentiating human B-lineage cells isolated from xenografted immunodeficient mice were generated. Comparison of these identified potentially clinically relevant features that both match and deviate from the normal profiles.

cancer biology↗

Zebrafish sp7 mutants show tooth cycling independent of attachment, eruption and poor differentiation of teeth

The capacity to fully replace teeth continuously makes zebrafish an attractive model to explore regeneration and tooth development. The requirement of attachment bone for the appearance of replacement teeth has been hypothesized but not yet investigated. The transcription factor sp7 (osterix) is known in mammals to play an important role during odontoblast differentiation and root formation. Here we study tooth replacement in the absence of attachment bone using sp7 zebrafish mutants. We analysed the pattern of tooth replacement at different stages of development and demonstrated that in zebrafish lacking sp7, attachment bone is never present, independent of the stage of tooth development or fish age, yet replacement is not interrupted. Without bone of attachment we observed abnormal orientation of teeth, and abnormal connection of pulp cavities of predecessor and replacement teeth. Mutants lacking sp7 show arrested dentinogenesis, with non-polarization of odontoblasts and only a thin layer of dentin deposited. Osteoclast activity was observed in sp7 mutants; due to the lack of bone of attachment, remodelling was diminished but nevertheless present along the pharyngeal bone. We conclude that tooth replacement is ongoing in the sp7 mutant despite poor differentiation and defective attachment. Without bone of attachment tooth orientation and pulp organization are compromised.

developmental biology↗

Regulator of calcineurin-2 is a ciliary protein with a role in cilia length control.

Almost every cell in the human body extends a primary cilium. Defective cilia function leads to a set of disorders known as ciliopathies characterised by debilitating developmental defects affecting many tissues. Here we report a new role for regulator of calcineurin 2, RCAN2, in primary cilia function. It localises to centrioles and the basal body and is required to maintain normal cilia length. RCAN2 was identified as the most strongly upregulated gene from a comparative RNAseq analysis of cells in which expression of the Golgi matrix protein giantin had been abolished by gene editing. In contrast to previous work where we showed that depletion of giantin by RNAi results in defects in ciliogenesis and in cilia length control, giantin knockout cells generate normal cilia on serum withdrawal. Furthermore, giantin knockout zebrafish show increased expression of RCAN2. Importantly, suppression of RCAN2 expression in giantin knockout cells results in the same defects in cilia length control seen on RNAi of giantin itself. Together these data define RCAN2 as a regulator of cilia function that can compensate for loss of giantin function.

cell biology↗

Giantin Knockout Models Reveal The Capacity Of The Golgi To Regulate Its Biochemistry By Controlling Glycosyltransferase Expression

The Golgi is the cellular hub for complex glycosylation, controlling accurate processing of complex proteoglycans, receptors, ligands, and glycolipids. Its structure and organisation is dependent on golgins, which tether cisternal membranes and incoming transport vesicles. Here we show that knockout of the largest golgin, giantin, leads to substantial changes in gene expression despite only limited effects on Golgi structure. Notably, 22 Golgi-resident glycosyltransferases, but not glycan processing enzymes or the ER glycosylation machinery, are differentially expressed following giantin ablation. This includes near-complete loss-of-function of GALNT3 in both mammalian cell and zebrafish models. Giantin knockout zebrafish exhibit hyperostosis and ectopic calcium deposits, recapitulating phenotypes of hyperphosphatemic familial tumoral calcinosis, a disease caused by mutations in GALNT3. These data reveal a new feature of Golgi homeostasis, the ability to regulate glycosyltransferase expression to generate a functional proteoglycome.\n\nSummary statementKnockout of giantin in a genome-engineered cell line and zebrafish models reveals the capacity of the Golgi to control its own biochemistry through changes in gene expression.

cell biology↗