La traduction des noms propres : une étude en corpus

Dans cet article, nous abordons le problème de la traduction des noms propres. Nous présentons notre hypothèse, selon laquelle la thèse très répandue de la non-traductibilité des noms propres peut être contredite. Puis, nous décrivons la construction du corpus multilingue aligné que nous utilisons pour illustrer notre propos. Nous évaluons enfin les apports et les limites de ce corpus dans le cadre de notre étude.The translation of proper names : a corpus study In this paper, we tackle the problem of the translation of proper names. We introduce our hypothesis according to which proper names can be translated more often than most people seem to think. Then, we describe the construction of a parallel multilingual corpus used to illustrate our point. We eventually evaluate both the advantages and limits of this corpus in our study

Classical cadherins control nucleus and centrosome position and cell polarity

Control of cell polarity is crucial during tissue morphogenesis and renewal, and depends on spatial cues provided by the extracellular environment. Using micropatterned substrates to impose reproducible cell–cell interactions, we show that in the absence of other polarizing cues, cell–cell contacts are the main regulator of nucleus and centrosome positioning, and intracellular polarized organization. In a variety of cell types, including astrocytes, epithelial cells, and endothelial cells, calcium-dependent cadherin-mediated cell–cell interactions induce nucleus and centrosome off-centering toward cell–cell contacts, and promote orientation of the nucleus–centrosome axis toward free cell edges. Nucleus and centrosome off-centering is controlled by N-cadherin through the regulation of cell interactions with the extracellular matrix, whereas the orientation of the nucleus–centrosome axis is determined by the geometry of N-cadherin–mediated contacts. Our results demonstrate that in addition to the specific function of E-cadherin in regulating baso-apical epithelial polarity, classical cadherins control cell polarization in otherwise nonpolarized cells

IFITM proteins inhibit placental syncytiotrophoblast formation and promote fetal demise

Comment in Protecting fetal development. [Science. 2019]International audienceElevated levels of type I interferon (IFN) during pregnancy are associated with intrauterine growth retardation, preterm birth, and fetal demise through mechanisms that are not well understood. A critical step of placental development is the fusion of trophoblast cells into a multinucleated syncytiotrophoblast (ST) layer. Fusion is mediated by syncytins, proteins deriving from ancestral endogenous retroviral envelopes. Using cultures of human trophoblasts or mouse cells, we show that IFN-induced transmembrane proteins (IFITMs), a family of restriction factors blocking the entry step of many viruses, impair ST formation and inhibit syncytin-mediated fusion. Moreover, the IFN inducer polyinosinic:polycytidylic acid promotes fetal resorption and placental abnormalities in wild-type but not in Ifitm-deleted mice. Thus, excessive levels of IFITMs may mediate the pregnancy complications observed during congenital infections and other IFN-induced pathologies