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Kennedy, M. J.

Publications and source records attributed to Kennedy, M. J..

4 recordsLinked to original sources

Development of a Norway Rat Hepacivirus Reporter for High-Throughput Quantification of Neutralising Antibodies

Hepatitis C virus (HCV) remains a major global health challenge, with vaccine research hindered by lack of immunocompetent animal models. Infection with the HCV-related Norway rat hepacivirus 1 (NrHV) in rats or mice shares HCV defining characteristics, including chronicity, delayed immune responses, and liver disease, thereby providing immunocompetent small animal models for immune responses and pathology. Infectious NrHV cell culture systems allow studies of host factors and neutralising antibodies, however, quantification relies on laborious manual counting of infected cells. To permit high-throughput quantification, we engineered culture adapted NrHV to encode green fluorescent protein (GFP), firefly luciferase (FLuc), or the 11 amino acid HiBiT tag at sites corresponding to those permissive for HCV. While GFP and FLuc constructs were not viable, a reporter with a HiBiT insertion in NS5A domain III was replication competent and produced infectious virus in rat hepatoma cells. Two mutations in NS5A adapted this virus to levels comparable to wildtype, enabling robust luciferase readouts and stability. The NrHV-HiBiT-NS5A reporter was viable in rats and permitted quantification of luciferase from liver homogenates. Luciferase-based quantification of viral infection after antibody neutralisation correlated well with manual quantification. High-throughput luciferase quantification was also used to confirm dependency on the known host factors SR-BI and miR-122, and to assess sensitivity to antivirals. Finally, sensitivity to a specific inhibitor suggested that cyclophilin A, similarly to HCV, may also be a host factor for NrHV. This novel reporter system could accelerate characterisation of the NrHV model as well as ongoing vaccine studies for HCV. ImportanceDirect acting antiviral therapy provides an effective cure for hepatitis C virus (HCV) infection, but the infection burden remains high due to cost, availability of therapy, and low diagnosis rates. A vaccine therefore is critical for global control of transmission, however development is constrained by a lack of immunocompetent animal models. Norway rat hepacivirus 1 (NrHV) infection of rats and mice serves as an effective small animal model for HCV, permitting evaluation of vaccine platforms and candidates. Neutralising antibody responses are considered crucial in protection and can be quantified using the NrHV cell culture system, however, only through laborious low-throughput methods. We here present an NrHV reporter virus allowing high-throughput quantification of antibody neutralisation, virus-host interactions, and antiviral efficacy via luciferase readout. This reporter will facilitate characterisation of NrHV and support ongoing vaccine research with the potential for global control of HCV.

microbiology↗

miRNA-mediated control of gephyrin synthesis drives sustained inhibitory synaptic plasticity

Activity-dependent protein synthesis is crucial for many long-lasting forms of synaptic plasticity. However, our understanding of the translational mechanisms controlling inhibitory synapses is limited. One distinct form of inhibitory long-term potentiation (iLTP) enhances postsynaptic clusters of GABAARs and the primary inhibitory scaffold, gephyrin, to promote sustained synaptic strengthening. While we previously found that persistent iLTP requires mRNA translation, the precise mechanisms controlling gephyrin translation during this process remain unknown. Here, we identify miR153 as a novel regulator of Gphn mRNA translation which controls gephyrin protein levels and synaptic clustering, ultimately impacting GABAergic synaptic structure and function. We find that iLTP induction downregulates miR153, reversing its translational suppression of Gphn mRNA and allowing for increased de novo gephyrin protein synthesis and synaptic clustering during iLTP. Finally, we find that reduced miR153 expression during iLTP is driven by an excitation-transcription coupling pathway involving calcineurin, NFAT and HDACs, which also controls the miRNA-dependent upregulation of GABAARs. Overall, this work delineates a miRNA-dependent post-transcriptional mechanism that controls the expression of the key synaptic scaffold, gephyrin, and may converge with parallel miRNA pathways to coordinate gene upregulation to maintain inhibitory synaptic plasticity.

neuroscience↗

Neurexin-3 defines synapse- and sex-dependent diversity of GABAergic inhibition in ventral subiculum

Ventral subiculum (vSUB) is integral to the regulation of stress and reward, however the intrinsic connectivity and synaptic properties of the inhibitory local circuit are poorly understood. Neurexin-3 (Nrxn3) is highly expressed in hippocampal inhibitory neurons, but its function at inhibitory synapses has remained elusive. Using slice electrophysiology, imaging, and single-cell RNA sequencing, we identify multiple roles for Nrxn3 at GABAergic parvalbumin (PV) interneuron synapses made onto vSUB regular spiking (RS) and burst spiking (BS) principal neurons. Surprisingly, we found that intrinsic connectivity and synaptic function of Nrxn3 in vSUB are sexually dimorphic. We reveal that vSUB PVs make preferential contact with RS neurons in males, but BS neurons in females. Furthermore, we determined that despite comparable Nrxn3 isoform expression in male and female PV neurons, Nrxn3 maintains synapse density at PV-RS synapses in males, but suppresses presynaptic release at the same synapses in females. HighlightsO_LIOverall inhibitory strength in ventral subiculum is cell-type specific C_LIO_LIPV circuits in ventral subiculum are organized sex-specifically C_LIO_LINrxn3 function in PV interneurons depends on postsynaptic cell identity C_LIO_LINrxn3 has distinct functions at PV-RS synapses in females compared to males C_LI O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=143 SRC="FIGDIR/small/440943v1_ufig1.gif" ALT="Figure 1"> View larger version (59K): org.highwire.dtl.DTLVardef@7fcf99org.highwire.dtl.DTLVardef@1167f82org.highwire.dtl.DTLVardef@d5c79org.highwire.dtl.DTLVardef@1320f09_HPS_FORMAT_FIGEXP M_FIG Graphical Abstract C_FIG

neuroscience↗

Local neuronal secretory trafficking dynamics revealed with zapERtrap: a light-inducible ER release system

For normal synapse and circuit function, neurons must regulate the abundance and localization of transmembrane receptor, channel and adhesion proteins over vast cellular expanses, including remote sites in dendrites and axons. Whether the secretory network can support long-range trafficking of synaptic proteins synthesized in the cell body or precise trafficking of locally generated proteins at remote sites remains poorly characterized. We developed an approach for locally triggering secretory trafficking from specific subcellular domains to explore the rate, activity dependence and cargo-specificity of central and remote trafficking networks. Surprisingly, different postsynaptic proteins processed in the cell body were transported deep into dendrites, but with strikingly different kinetics, spatial distributions and activity dependencies. Proteins locally processed in dendrites were broadly dispersed prior to surface insertion, but could be directed locally to synapses. These results provide a novel interrogation of compartmentalized trafficking and reveal basic principles for protein targeting in complex cellular environments.

cell biology↗