Publications by authors named "M Schertzer"

Article Synopsis
  • - Epithelial-to-mesenchymal transition (EMT) is a process that helps cancer cells spread (metastasize) and become resistant to cell death and treatments, but the triggers for EMT are not well understood
  • - The study shows that DNA damage activates specific proteins (PARP and ALC1), which help EMT transcription factors access DNA, leading to changes in cell behavior and enhanced ability to repair DNA
  • - Using a PARP inhibitor can reverse or prevent EMT caused by DNA damage, and help make cancer cells more sensitive to other treatments, offering potential new strategies for cancer therapy
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Regulator of TElomere Length Helicase 1 (RTEL1) is a helicase required for telomere maintenance and genome replication and repair. RTEL1 has been previously shown to participate in the nuclear export of small nuclear RNAs. Here we show that RTEL1 deficiency leads to a nuclear envelope destabilization exclusively in cells entering S-phase and in direct connection to origin firing.

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This work investigates the deposition patterns left by evaporating particle-laden droplets on heterogeneous surfaces with spatially varying wettability. Spatial differences in receding contact angles give rise to scalloped-shaped contact lines. During evaporation, the contact line recedes in one location and remains pinned in another.

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Alternative splicing is an essential mechanism for diversifying proteins, in which mature RNA isoforms produce proteins with potentially distinct functions. Two major challenges in characterizing the cellular function of isoforms are the lack of experimental methods to specifically and efficiently modulate isoform expression and computational tools for complex experimental design. To address these gaps, we developed and methodically tested a strategy which pairs the RNA-targeting CRISPR/Cas13d system with guide RNAs that span exon-exon junctions in the mature RNA.

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During mouse embryogenesis, expression of the long non-coding RNA (lncRNA) Airn leads to gene repression and recruitment of Polycomb repressive complexes (PRCs) to varying extents over a 15-Mb domain. The mechanisms remain unclear. Using high-resolution approaches, we show in mouse trophoblast stem cells that Airn expression induces long-range changes to chromatin architecture that coincide with PRC-directed modifications and center around CpG island promoters that contact the Airn locus even in the absence of Airn expression.

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