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Maroilley, T.

Publications and source records attributed to Maroilley, T..

3 recordsLinked to original sources

Host genetics and pre-vaccination blood transcriptome as determinants of vaccine-induced immunity to Influenza A virus in swine

Influenza A virus (IAV) is a major respiratory pathogen in pigs, causing diseases that have significant economic and potential public health consequences. Vaccine effectiveness varies among animals, impacting long-term herd protection due to individual variabilities in antibody levels and persistence over time. Our aim was to identify the genetic factors and pre-vaccination blood transcriptomic profiles that influence immune response levels to the IAV vaccine. A total of 187 piglets were vaccinated at weaning (28 days of age, 0 days post-vaccination, dpv) and boosted three weeks later, and humoral responses were assessed until slaughter (21, 28, 35, and 118 dpv) by measuring serum IAV-specific IgG and hemagglutination inhibition (HAI) titers. The results revealed varying antibody responses and persistence. Genome-wide association studies identified two loci on chromosomes SSC5 and SSC8 associated with a persistence of HAI titers until slaughter. Pre-vaccination blood transcriptomic analyses showed that early and post-boost antibody responses (21, 28 and 35 dpv) and long-term persistence (118 dpv) were associated with distinct baseline immune programs, with extracellular matrix and myeloid-related signatures predicting strong early and peak responses, whereas interferon-related signatures were linked to reduced long-term antibody persistence. Our results highlight the importance of considering the role of immune competence and genetics in vaccine responses in pigs and suggest candidate biomarkers to improve vaccination strategies within breeding programs.

genomics↗

A Course-Undergraduate Research Experience (CURE) to explore the effect of structural variants on gene expression in C. elegans balancers

Bioinformatics, a discipline at the crossroads of Biology and Computational Sciences, also referred to as Computational Biology, is nowadays widely spread in research programs. However, implementing any Bioinformatics projects requires the ability to comprehend biological concepts and apply computational approaches, and rare are the undergraduate programs offering such multi-disciplinary training. In addition, understanding the dynamic between Biology research projects and Bioinformatics analyses is challenging with no real-life experience. Course-based undergraduate research experience (CURE) courses are innovative programs that allow more students to acquire research experience and provide the perfect setting to introduce students to applied bioinformatics. As a part of the Bachelor of Health Sciences of the Cumming School of Medicine at the University of Calgary (Canada), a CURE applied bioinformatics was implemented in the Winter of 2023 to 2025. Students investigated the effect of structural variants (SVs, genetic variants larger than 50 bp) on gene expression in the model organism Caenorhabditis elegans (a hermaphrodite 1-mm long roundworm). The students detected and characterized SVs by analyzing genome and transcriptome sequencing data of C. elegans strains called balancers, as they are known to carry large genomic variations balancing regions of the genome by limiting recombination and allowing maintenance of lethal mutations. They used Galaxy, a public web-based supercomputing resource, but also a local High-Performance computing system, and R, to report different effects of SVs on gene expression and splicing. Students research explained the molecular mechanism behind the uncoordinated phenotype caused by the reciprocal translocation eT1(III;V) and uncovered unexpected effects on gene expression on an understudied gene. We evaluated the courses impact on student learning journeys and showed that the CURE favored students understanding of the Bioinformatics field and fostered their research interest. We provide here guidelines to facilitate the CURE implementations to improve access for undergraduate students to bioinformatics research experiences.

bioinformatics↗

FMRP controls diacylglycerol-dependent neuronal activity by mediating m6A-regulated translation efficiency

Fragile X syndrome (FXS), a leading inherited cause of intellectual developmental disorder and autism, results from loss of the RNA-binding protein FMRP. Loss of FMRP causes excessive neuronal protein synthesis contributing to widespread functional disturbances, yet the mechanisms linking FMRP to specific mRNA targets remain unclear. We show that FMRP promotes translation of the brain mRNA DGK{kappa} by binding mA-modified repetitive RNA motifs, thereby relieving a translational block encoded within its sequence. FMRP loss sharply reduces neuronal DGK{kappa}, and DGK{kappa} depletion alone reproduces hallmark FXS phenotypes, including hyperactivity, compulsive behavior, overgrowth, dendritic spine abnormalities, overactivated diacylglycerol signaling and increased protein synthesis. These findings identify DGK{kappa} as a key effector of FMRP function and establish a regulatory axis where mA RNA modification modulates neuronal translation. This work defines new principles of translational control in neurodevelopmental disorders and positions DGK{kappa} as a central driver of FXS pathogenesis.

molecular biology↗