Laboratoire de Biologie Moléculaire et Cellulaire des Eucaryotes
Laboratory of Molecular and Cellular Biology of Eukaryotes
« Réponses Moléculaire et Cellulaire au télomère les plus court chez Saccharomyces cerevisiae » dirigée par Dr Teresa Teixeira
La soutenance se tiendra le vendredi 11 Octobre 2024 à 14h, dans la Bibliothèque Edmond de Rothschild de l’Institut de Biologie Physico-Chimique (IBPC) au 13 rue Pierre et Marie Curie 75005, Paris
Telomeres, the natural ends of chromosomes, resemble double-strand breaks (DSBs) and require protection by the shelterin complex to prevent aberrant activation of the DNA damage response (DDR) in somatic cells.
Outer mitochondrial membrane fusion, a vital cellular process, is mediated by mitofusins. However, the underlying molecular mechanism remains elusive.
Telomere maintenance is a universal hallmark of cancers to sustain the unlimited proliferative potential. In ~85% of cancers, telomere shortening is mitigated by reactivated telomerase expression while the other ~15% use a recombination-based mechanism, termed Alternative Lengthening of Telomeres (ALT)
Replicative senescence is triggered when telomeres reach critically short length and activate permanent DNA damage checkpoint-dependent cell cycle arrest.
Mitofusins are large GTPases that trigger fusion of mitochondrial outer membranes. Similarly to the human mitofusin Mfn2, which also tethers mitochondria to the endoplasmic reticulum (ER), the yeast mitofusin Fzo1 stimulates contacts between Peroxisomes and Mitochondria when overexpressed.
Identification of Cellular Protein Targets of a Half-Sandwich Iridium (III) Complex Reveals Its Dual Mechanism of Action via Both Electrophilic and Oxidative Stresses Robin Ramos , Anthi Karaiskou, Candice Botuha, Sadek Amhaz, Michaël Trichet, Florent Dingli, Jérémy Forté, France Lam, Read more
Individual cell fate and population dynamics revealed by a mathematical model linking telomere length and replicative senescence A. Rat, M. Doumic, M. T. Teixeira and Z. Xu. Progressive shortening of telomeres ultimately causes replicative senescence and is linked with aging Read more
« Hog1 acts in a Mec1-independent manner to counteract oxidative stress following telomerase inactivation » Bechara Zeinoun, Maria Teresa Teixeira and Aurélia Barascu Replicative senescence is triggered when telomeres reach critically short length and activate permanent DNA damage checkpoint-dependent cell cycle arrest. Read more
« Replicative senescence-associated oxidative stress and Hog1 activation in telomerase negative Saccharomyces cerevisiae cells » dirigée par Dr Teresa Teixeira et Dr Aurélia Barascu
La soutenance aura lieu le vendredi 8 décembre à 14h dans dans la bibliothèque Edmond de Rothschild de l’IBPC.