Michael D. Wilson

The paper presents a telomere-to-telomere genome assembly of the naked mole-rat and compares it with a related species to identify gene losses and duplications associated with unique traits.

The paper uses long-read sequencing to detect transgene concatenation and off-target integration in a mouse model, revealing hidden genomic complexity and phenotypic disruption.

This study identifies the ARP2/3 complex as a downstream effector of mTORC1 and mTORC2 hyperactivation in PTEN-deficient neural cells, showing its inhibition can rescue disease phenotypes.

The paper identifies TOP2B binding sites as mutational hotspots in cancer genomes, showing their role in structural variants and driver mutations in genes like TP53 and MYC.

This study evaluates how blood transcriptome profiling adds value to genome sequencing in diagnosing rare genetic disorders in a pediatric cohort.

The paper shows that the nuclear fragment of fat cadherin, generated by cleavage, regulates gene expression by interacting with Hippo pathway components and other factors.

The paper presents an updated reference genome for the naked mole-rat, identifying gene losses and gains linked to its unique physiological traits.

This paper shows C9orf72 expansions create a folate-sensitive fragile site FRA9A, leading to chromosomal instability and immune responses in patient cells and mice.

The paper analyzes hypothalamic gene expression in mice across puberty, identifying age- and sex-specific changes and their association with pubertal regulation.

The paper assesses the impact of rare canonical splice site variants on splicing using functional and in silico methods, finding that 24% of variants do not cause loss-of-function.

The paper investigates how mRNA half-life buffers transcription rate changes in Rett syndrome models, identifying post-transcriptional mechanisms in human and mouse neurons.

The paper measures transcription rate and mRNA half-life changes during human neuronal development and identifies transcriptional buffering as the most prevalent mode of gene regulation.

The paper develops DEET, a tool that reanalyzes differential gene expression data from multiple studies to help users compare their gene lists with existing results.

Amniotic fluid stem cell extracellular vesicles improve fetal lung development in CDH by modulating macrophage inflammation and restoring normal gene expression.

The paper analyzes RELA-bound transposable elements across species to show their ancient and lineage-specific contributions to NF-κB binding and inflammation.

This study identifies GATA4/5/6 as conserved regulators of cardiac versus pharyngeal mesoderm fate by analyzing single-cell gene expression in zebrafish and Ciona.

This study profiles gene and miRNA expression in mouse pituitaries across postnatal ages to identify sex-biased gene regulation and cell-type proportion differences during development.

The paper identifies TIA1 mRNA targets during human neuronal development and shows that TIA1 binding is associated with translation repression and neurodevelopmental gene regulation.

scMappR assigns cell-type specificity scores to bulk RNA-seq DEGs using scRNA-seq data and deconvolution methods, showing accurate assignment in kidney regeneration analysis.

The paper demonstrates that extracellular vesicles from amniotic fluid stem cells can rescue impaired fetal lung development in experimental models.

The paper identifies epigenetic activation of contractility-driving genes in the mouse myometrium before labor onset, revealing early H3K27ac enrichment and transcriptional changes during active labor.

The paper curates a database of human brain RNA-seq metadata to improve reproducibility and analysis of gene expression data.

The paper identifies conserved enhancers active early in zebrafish heart development that recapitulate human expression patterns, suggesting ancient regulatory mechanisms.

This study shows Hey2 restricts SHF progenitor addition to the zebrafish heart, preventing excessive myocardial cell growth and congenital heart defects.