Publications by authors named "Claire Ghilain"
Article Synopsis
- Linear DNA can't hold supercoils due to its free rotation at the ends, but mammalian telomeres can because they face topological stress.
- Previous studies observed negative supercoiling in telomeres, but positive supercoils weren't investigated until now due to the lack of proper tools.
- New tools developed in this study revealed that replication stress and Topoisomerase 2 inhibition led to positive supercoil build-up at telomeres and the FRA3B fragile site, suggesting a model for DNA fragility.
Protecting telomere from the DNA damage response is essential to avoid the entry into cellular senescence and organismal aging. The progressive telomere DNA shortening in dividing somatic cells, programmed during development, leads to critically short telomeres that trigger replicative senescence and thereby contribute to aging. In several organisms, including mammals, telomeres are protected by a protein complex named Shelterin that counteract at various levels the DNA damage response at chromosome ends through the specific function of each of its subunits.
View Article and Find Full Text PDFImpaired adipose tissue insulin signalling is a critical feature of insulin resistance. Here we identify a pathway linking the lipolytic enzyme hormone-sensitive lipase (HSL) to insulin action via the glucose-responsive transcription factor ChREBP and its target, the fatty acid elongase ELOVL6. Genetic inhibition of HSL in human adipocytes and mouse adipose tissue results in enhanced insulin sensitivity and induction of ELOVL6.
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