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Gupta, Y.

Publications and source records attributed to Gupta, Y..

10 recordsLinked to original sources

Beyond the Axenic Culture Filtrate Secretome: BONCAT and conventional proteomics together reveal the Infection-associated secreted protein repertoire of Acinetobacter baumannii in the human lung Epithelial cell line A549

Acinetobacter baumannii (Ab) is an important opportunistic pathogen responsible for pneumonia, bloodstream infections, and sepsis. Although several virulence determinants have been characterized, the bacterial secreted protein repertoire associated with host cell infection remains incompletely understood. Conventional proteomic analyses of axenic cultures provide valuable information but cannot distinguish proteins synthesized before infection from those produced during host pathogen interactions. This study combined bioorthogonal noncanonical amino acid tagging (BONCAT) with conventional proteomics to characterize the infection associated Ab secreted protein repertoire recovered from human lung epithelial A549 cells. To achieve pathogen selective metabolic labelling, an Ab clinical isolate that had caused neonatal sepsis (Ab7) was engineered to express a methionyl tRNA synthetase variant, MetRSNLL (L10N, Y258L, H299L), capable of incorporating azidonorleucine (ANL) into newly synthesised bacterial proteins. Labelling conditions were optimized using methionine biosynthesis inhibitory amino acids, which reduced endogenous methionine availability without appreciably affecting bacterial growth. Efficient ANL incorporation was confirmed by flow cytometry, confocal microscopy, biotin streptavidin assays, and in gel fluorescence. Metabolic labelling also remained compatible with bacterial intracellular survival. Sequential labelling with azidohomoalanine (AHA) before infection and ANL during A549 infection enabled the temporal assignment of bacterial protein synthesis. Subsequent SDS PAGE fractionation and LC MS/MS identified 152 infection-associated proteins, including 23 containing experimentally detected amino acid analogue modifications. Among these, 13 were AHA only, nine were ANL only, and one contained both analogues. Notably, 117 proteins were not detected in either axenic reference proteome. The infection associated fraction exhibited enrichment of predicted signal peptide containing and outer membrane proteins, while functional annotation identified enrichment of bacterial secretion system components among infection-only proteins. These findings demonstrate the complementary strengths of BONCAT and conventional proteomics: BONCAT provides evidence of bacterial protein synthesis during infection, whereas conventional proteomics expands detection beyond proteins containing identifiable analogue modified peptides. Although extracellular recovery does not establish active secretion, the combined approach reveals a host associated bacterial protein repertoire extending beyond axenic observations. This framework supports future investigations into bacterial adaptation, host pathogen interactions, and the prioritization of candidate diagnostic biomarkers, subject to functional characterization and clinical validation. The study establishes a methodological foundation for investigating infection-associated protein synthesis and release in complex host pathogen environments.

microbiology↗

Increases in therapist-patient physiological synchrony after dog-patient contact in canine-assisted psychotherapy: an exploratory pilot study

Introduction: Canine-assisted psychotherapy (CAP) introduces a therapy dog into the therapist-patient relationship and may influence interpersonal processes underlying therapeutic change. This exploratory pilot study investigated whether direct patient-dog contact is associated with changes in autonomic arousal and therapist-patient physiological synchrony. Methods: Skin conductance was recorded from 18 patients with depressive disorders and one therapist during 53 routine CAP sessions. A total of 192 episodes of direct patient-dog contact were identified from video recordings. Three-minute periods before and after each contact onsets were compared. Skin conductance level (SCL), skin conductance fluctuations (SCF), and therapist-patient physiological synchrony were assessed using zero-lag correlation and maximum cross-correlation. Sliding-window analyses examined temporal changes in synchrony, while randomly selected pseudo-events served as controls. Results: SCL increased significantly following dog contact in both patients and the therapist, whereas SCF rate over 3 min did not change significantly. Therapist-patient physiological synchrony increased significantly after dog contact, as indicated by both zero-lag correlation and maximum cross-correlation. Sliding-window analyses confirmed these increases and showed a reduction in the temporal lag between the two physiological signals. Importantly, increases in synchrony were significantly greater following genuine dog-contact events than following pseudo-events. Discussion: Direct physical contact between patients and therapy dogs is followed by increased autonomic arousal and enhanced therapist-patient physiological synchrony. These findings suggest that dog-patient contact may function as an interactional event that promotes physiological coordination and interpersonal attunement within the therapeutic dyad.

physiology↗

Identification and characterization of a SARS-CoV-2 Mpro G23 deletion ensitrelvir-resistant mutant

Ensitrelvir is an antiviral drug that specifically targets the main protease (Mpro) of Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has been approved for the treatment of coronavirus disease 2019 (COVID-19) due to the conservation of its target protein which is essential in the viral lifecycle. However, SARS-CoV-2 could introduce mutations in the viral proteins to confer resistance to antivirals. Thus, screening for drug-resistant SARS-CoV-2 mutants and elucidating their resistant mechanisms are critical for guiding the selection of effective antiviral therapies. Here, we utilized a luminescent attenuated SARS-CoV-2 ({Delta}3a7b-Nluc WT) to safely identify ensitrelvir drug-resistant mutants (DRM-E) without the need of using virulent forms of SARS-CoV-2. We isolated a DRM-E containing a G23 deletion (G23del) in Mpro with high resistance (>1,000 fold) to ensitrelvir, but not to the other Mpro inhibitor (nirmatrelvir) or to the RNA-dependent RNA polymerase (RdRp) inhibitor remdesivir. The contribution of G23del was confirmed by generating a recombinant luminescent attenuated SARS-CoV-2 containing G23del in the non-structural protein 5 (NSP5) gene ({Delta}3a7b-Nluc G23del). {Delta}3a7b-Nluc G23del exhibited significant resistance to ensitrelvir in both cultured cells an in K18 hACE2 transgenic mice. Binding affinity revealed that G23del mutation substantially altered Mpro binding affinity for ensitrelvir but not nirmatrelvir. In conclusion, our results demonstrate that G23del in Mpro can confer high resistance to ensitrelvir. Positively, G23del in Mpro does not render SARS-CoV-2 resistant to nirmatrelvir or remdesivir, suggesting the feasibility of treating infections with SARS-CoV-2 containing G23del with these other approved antivirals. SIGNIFICANCEThe clinical use of SARS-CoV-2 antiviral drugs is increasingly challenged by the emergence of drug-resistant mutants. Thus, there is a pressing need to identify and characterize antiviral escape SARS-CoV-2 variants, particularly for FDA-approved antivirals. Our study addresses this by employing a luminescent attenuated virus platform ({Delta}3a7b-Nluc WT) to safely identify and characterize resistance mutations without the concern of using virulent forms of SARS-CoV-2. Using this safe approach, we have identified a G23 deletion (G23del) in SARS-CoV-2 Mpro, which mediates resistance to ensitrelvir in vitro and in vivo. Importantly, while G23del was able to confer more than 1,000-fold increased resistance to ensitrelvir, SARS-CoV-2 containing G23del remained sensitive to other Mpro (nirmatrelvir) and RdRp (remdesivir) inhibitors. Altogether, this study demonstrates the feasibility of using {Delta}3a7b-Nluc to safely identify and characterize drug resistant viruses without the biosafety concern of using virulent SARS-CoV-2 and advance the design of next-generation antiviral drugs.

microbiology↗

Controlled decorin delivery from injectable microgels promotes scarless vocal fold repair

Vocal fold (VF) scarring is a leading cause of poor voice, yet no therapies exist to prevent its progression. Current treatments, such as intracordal steroid injections, offer limited efficacy and carry significant off-target toxicities. To identify targeted anti-scarring strategies, we performed transcriptomics of human VF myofibroblasts, the cellular drivers of VF scarring, and identified the proteoglycan decorin (DCN) as downregulated in activated myofibroblasts. We also show a time-dependent decrease in DCN during fibrotic wound healing in a preclinical rat model of VF scarring. Administration of DCN suppressed VF myofibroblast activation by reducing pro-fibrotic gene expression, -smooth muscle actin (-SMA) levels, and cell contractility. DCN was encapsulated in hyaluronic acid microgels for sustained protein release for 3-4 weeks. In a rat model of VF scarring, DCN-loaded microgels prevented hallmark features of scarring, including collagen deposition and myofibroblast activation. These findings highlight DCN as a promising therapeutic and provide a sustained delivery platform with translational potential against VF scarring. TeaserControlled decorin drug delivery from hyaluronic acid microgels attenuates myofibroblast activation to prevent vocal fold scarring, offering a translational strategy to improve post-injury voice outcomes.

bioengineering↗

Patient-specific iPSC models of neural tube defects identify underlying deficiencies in neuroepithelial cell shape regulation and differentiation

Spina bifida and anencephaly are neural tube defects caused by failure of embryonic neural tube closure. Successful closure requires apicobasal elongation and apical constriction of neuroepithelial cells. These critical behaviours have not been studied in human, patient-specific models. We characterise a human iPSC-derived neuroepithelial morphogenesis model that is highly reproducible across three parental iPSC lines of diverse origin and reprogramming technologies. Differentiated neuroepithelial cells actively undergo ROCK-dependent apical constriction. ROCK acts downstream of planar cell polarity/VANGL2 in other species. We find that VANGL2 is up-regulated and phosphorylated during iPSCs-to-neuroepithelial differentiation. The patient-identified VANGL2-R353C mutation does not alter VANGL2 expression, localisation or phosphorylation, but reduces myosin-II phosphorylation and apical constriction relative to congenic control iPSCs. Non-congenic comparisons and forward genetic testing are also informative in this reproducible model. We compare lines reprogrammed from amniocytes of two patients with spina bifida, versus two controls. One patient-derived line forms a morphologically normal neuroepithelium, but fails to differentiate into neurons. The second fails to undergo apicobasal elongation, and harbours compound heterozygous mutations in the MED24 gene previously implicated in neuroepithelial elongation in mice. Thus, iPSC-derived neuroepithelial modelling reveals mechanistic insights into conserved cell behaviours, including apical constriction, apicobasal elongation and neural differentiation, links genetically-impaired apical constriction to human disease, and establishes patient-specific models which recapitulate failures across these heterogenous neuroepithelial functions.

developmental biology↗

Generation of C9orf72 repeat knock-in iPSC lines for modelling ALS and FTD

Induced pluripotent stem cell (iPSC) models are powerful tools for neurodegenerative disease modelling, as they allow mechanistic studies in a human genetic environment and they can be differentiated into a range of neuronal and non-neuronal cells. However, these models come with inherent challenges due to line-to-line and clonal variability. To combat this issue, the iPSC Neurodegenerative Disease Initiative (iNDI) has generated an iPSC repository using a single clonal reference line, KOLF2.1J, into which disease-causing mutations and revertants are introduced via gene editing. Here we describe the generation and validation of lines carrying the most common causative mutation for amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), a repeat expansion in the C9orf72 gene, for the iNDI collection of neurodegenerative iPSC models. We demonstrate that these C9orf72 knock-in lines differentiate efficiently into neurons and display characteristic C9orf72-associated pathologies, including reduced C9orf72 levels and the presence of dipeptide repeat proteins (DPRs) and RNA foci, which increase in abundance over time in culture. These pathologies are not present in revertant cells lacking the repeat expansion. These repeat expansion and revertant cell lines are now available to academic and for-profit institutions through the JAX iPS cell repository and will help to facilitate and standardise iPSC-based ALS/FTD research.

neuroscience↗

Structural Insights into the Assembly and Regulation of 2'-O RNA Methylation by SARS-CoV-2 nsp16/nsp10

2-O-ribose methylation of the first transcribed base (adenine or A1 in SARS-CoV-2) of viral RNA mimics the host RNAs and subverts the innate immune response. How nsp16, with its obligate partner nsp10, assembles on the 5-end of SARS-CoV-2 mRNA to methylate the A1 has not been fully understood. We present a [~] 2.4 [A] crystal structure of the heterotetrameric complex formed by the cooperative assembly of two nsp16/nsp10 heterodimers with one 10-mer Cap-1 RNA (product) bound to each. An aromatic zipper-like motif in nsp16 and the N-terminal regions of nsp10 and nsp16 orchestrate an oligomeric assembly for efficient methylation. The front catalytic pocket of nsp16 stabilizes the upstream portion of the RNA while the downstream RNA remains unresolved, likely due to its flexibility. An inverted nsp16 dimer extends the positively charged surface area for longer RNA to influence the catalysis. Additionally, a non-specific nucleotide-binding pocket on the backside of nsp16 plays a critical role in catalysis, further contributing to its enzymatic activity.

microbiology↗

IRF8-mutant B cell lymphoma evades immunity through a CD74-dependent deregulation of antigen processing and presentation in MHC CII complexes

In diffuse large B-cell lymphoma (DLBCL), the transcription factor IRF8 is the target of a series of potentially oncogenic events, including, chromosomal translocation, focal amplification, and super-enhancer perturbations. IRF8 is also frequently mutant in DLBCL, but how these variants contribute to lymphomagenesis is unknown. We modeled IRF8 mutations in DLBCL and found that they did not meaningfully impact cell fitness. Instead, IRF8 mutants, mapping either to the DNA-binding domain (DBD) or c-terminal tail, displayed diminished transcription activity towards CIITA, a direct IRF8 target. In primary DLBCL, IRF8 mutations were mutually exclusive with mutations in genes involved in antigen presentation. Concordantly, expression of IRF8 mutants in murine B cell lymphomas uniformly suppressed CD4, but not CD8, activation elicited by antigen presentation. Unexpectedly, IRF8 mutation did not modify MHC CII expression on the cell surface, rather it downmodulated CD74 and HLA- DM, intracellular regulators of antigen peptide processing/loading in the MHC CII complex. These changes were functionally relevant as, in comparison to IRF8 WT, mice harboring IRF8 mutant lymphomas displayed a significantly higher tumor burden, in association with a substantial remodeling of the tumor microenvironment (TME), typified by depletion of CD4, CD8, Th1 and NK cells, and increase in T-regs and Tfh cells. Importantly, the clinical and immune phenotypes of IRF8-mutant lymphomas were rescued in vivo by ectopic expression of CD74. Deconvolution of bulk RNAseq data from primary human DLBCL recapitulated part of the immune remodeling detected in mice and pointed to depletion of dendritic cells as another feature of IRF8 mutant TME. We concluded that IRF8 mutations contribute to DLBCL biology by facilitating immune escape.

cancer biology↗

Antivirals against monkeypox infections

Monkeypox virus (MPXV) infection in humans are historically restricted to endemic regions in Africa. However, in 2022, an alarming number of MPXV cases have been reported globally with evidence of person-to-person transmission. Because of this, the World Health Organization (WHO) declared the MPXV outbreak a public health emergency of international concern. MPXV vaccines are limited and only two antivirals, tecovirimat and brincidofovir, approved by the United States (US) Food and Drug Administration (FDA) for the treatment of smallpox, are currently available for the treatment of MPXV infection. Here, we evaluated 19 compounds previously shown to inhibit different RNA viruses for their ability to inhibit Orthopoxvirus infections. We first used recombinant vaccinia virus (rVACV) expressing fluorescence (Scarlet or GFP) and luciferase (Nluc) reporter genes to identify compounds with anti-Orthopoxvirus activity. Seven compounds from the ReFRAME library (antimycin A, mycophenolic acid, AVN- 944, pyrazofurin, mycophenolate mofetil, azaribine, and brequinar) and six compounds from the NPC library (buparvaquone, valinomycin, narasin, monensin, rotenone, and mubritinib) showed antiviral activity against rVACV. Notably, the anti-VACV activity of some of the compounds in the ReFRAME library (antimycin A, mycophenolic acid, AVN- 944, mycophenolate mofetil, and brequinar) and all the compounds from the NPC library (buparvaquone, valinomycin, narasin, monensin, rotenone, and mubritinib) were confirmed with MPXV, demonstrating the broad-spectrum antiviral activity against Orthopoxviruses and their potential to be used for the antiviral treatment of MPXV, or other Orthopoxvirus, infections. IMPORTANCEDespite the eradication of smallpox, some Orthopoxviruses remain important human pathogens, as exemplified by the recent 2022 monkeypox virus (MPXV) outbreak. Although smallpox vaccines are effective against MPXV, there is presently limited access to those vaccines. In addition, current antiviral treatment against MPXV infections is limited to the use of the FDA-approved drugs tecovirimat and brincidofovir. Thus, there is an urgent need to identify novel antivirals for the treatment of MPXV, and other potentially zoonotic Orthopoxvirus infections. Here, we show that thirteen compounds, derived from two different libraries, previously found to inhibit several RNA viruses, exhibit also antiviral activity against VACV. Notably, eleven compounds also displayed antiviral activity against MPXV, demonstrating their potential to be incorporated into the therapeutic armamentarium to combat Orthopoxvirus infections.

microbiology↗

Low-level mitochondrial heteroplasmy modulates DNA replication, glucose metabolism and lifespan in mice

Mutations in mitochondrial DNA (mtDNA) lead to heteroplasmy, i.e. the intracellular coexistence of wild-type and mutant mtDNA strands, which impact a wide spectrum of diseases but also physiological processes, including endurance exercise performance in athletes. However, the phenotypic consequences of limited levels of naturally-arising heteroplasmy have not been experimentally studied to date. We hence generated a conplastic mouse strain carrying the mitochondrial genome of a AKR/J mouse strain (B6-mtAKR) together with a C57BL/6J nuclear genomic background, leading to >20% heteroplasmy in the origin of light-strand DNA replication (OriL). These conplastic mice demonstrate a shorter lifespan as well as dysregulation of multiple metabolic pathways, culminating in impaired glucose metabolism, compared to wild-type C57BL/6J mice carrying lower levels of heteroplasmy. Our results indicate that physiologically relevant differences in mtDNA heteroplasmy levels at a single, functionally important site impair metabolic health and lifespan in mice.\n\nHighlightsO_LIWe identify heteroplasmy of the adenine-repeat variation (9 to 13A) in nt5172 in the origin of light-strand DNA replication (OriL) in inbred mice.\nC_LIO_LIB6-mtAKR mice carry >20% 12A heteroplasmy in the OriL, while B6 mice carry only [~] 10% heteroplasmy.\nC_LIO_LIThe level of 12A heteroplasmy correlates to mtDNA copy number, glucose metabolism, and lifespan in mice.\nC_LIO_LIGiven the established role of mtDNA heteroplasmy in regards to endurance exercise performance in athletes, these findings may impact our understanding of metabolism and aging in humans.\nC_LI

genetics↗