5 research outputs found

    Prácticas resistentes en el México de la desaparición forzada

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    This article reflects on how practice of enforced disappearance ravishes the Mexican territory. Scrutinizing the State’s narrative strategy as a rhetorical assault on the possibility of legal and historical truth, which imposes oblivion, it analyzes parallel constructions of counter-truths that pressingly claim for immediate memory. Two cases are used as a starting point of the analysis: the Caravan of Central American Mothers crossing Mexico and the movement that arose as a result of the attack led against Ayotzinapa normalista students on September 26th, 2014, bringing into focus how their discourses and practices shatter the univocal official narrative. Finally, the article puts forward some considerations on the state of fear and violence pervading the country at present as well as a fundamental need to learn to call it by its name

    COQ4 is required for the oxidative decarboxylation of the C1 carbon of Coenzyme Q in eukaryotic cells

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    Pelosi L, Morbiato L, Burgardt A, et al. COQ4 is required for the oxidative decarboxylation of the C1 carbon of Coenzyme Q in eukaryotic cells. Molecular Cell. Accepted.Coenzyme Q (CoQ) is a redox lipid that fulfills critical functions in cellular bioenergetics and homeostasis. CoQ is synthesized by a multi-step pathway that involves several COQ proteins. Two steps of the eukaryotic pathway, the decarboxylation and hydroxylation of position C1, have remained uncharacterized. Here, we provide evidence that these two reactions occur in a single oxidative decarboxylation step catalyzed by COQ4. We demonstrate that COQ4 complements an Escherichia coli strain deficient for C1 decarboxylation and hydroxylation and that COQ4 displays oxidative decarboxylation activity in the non-CoQ producer Corynebacterium glutamicum. Overall, our results substantiate that COQ4 contributes to CoQ biosynthesis, not only via its previously proposed structural role, but also via oxidative decarboxylation of CoQ precursors. These findings fill a major gap in the knowledge of eukaryotic CoQ biosynthesis, and shed new light on the pathophysiology of human primary CoQ deficiency due to COQ4 mutations
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