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espanolResumen: En este trabajo se analiza el significado actual del deber de fidelidad en el contexto del Codigo Civil Espanol, a la vista de como es tratado por los tribunales. El establecimiento de un divorcio acausal ha significado un cambio en la valoracion de los deberes que incumben a los casados, no asociandose la separacion o divorcio con el incumplimiento de los deberes entre ellos, especialmente el de fidelidad. El argumento preferido del Tribunal Supremo consiste en negar las pretensiones de danos por infidelidad al existir una consecuencia legal especifica para ello, como la separacion. Sin embargo, este ha perdido su valor, dejando a los jueces inmersos en una posicion de incertidumbre. Asi, se ha ido abriendo camino una linea de resolucion particular que permite el reclamo de indemnizaciones por el hecho de que se oculte al otro conyuge la verdadera filiacion de los hijos, concebidos como resultado de la otra relacion constante de matrimonio. EnglishAbstract: This study analyses the contemporary meaning of the duty of fidelity in the context of the Spanish Civil Code, in terms of its treatment in court. The establishment of the no-fault divorce has led to a change in the value given to spousal duties, with separation or divorce not associated with the failure to fulfil said duties, especially those pertaining to fidelity. The argument preferred by the Supreme Court is based on the denial of claims for damages caused by infidelity. With the existence of a specific legal consequence for infidelity, such as separation, this argument has lost value. This has placed judges in a position of uncertainty, which led to the establishment of a private solution that allows the claim for compensation when one spouse has hidden from the other the true parentage of the children conceived as a result of the other constant/long-term relationship.

Background X-linked agammaglobulinemia (XLA) is characterized by impaired B-cell differentiation caused by mutations in the Bruton's tyrosine kinase (Btk) gene. The natural disease model, the X-linked immunodeficiency mouse, shows a less severe phenotype, indicating a different requirement of Btk in human and mouse B cells. Btk is also expressed in the myeloid line and participates in LPS signaling. Deficient oxidative burst and myeloid differentiation have been reported in the X-linked immunodeficiency mouse, but the precise mechanism and relevance of Btk activity in human monocytes is poorly understood. Objective The apparent absence in XLA of clinical manifestations of myeloid deficiency prompted us to explore the relevance of complete Btk absence in human myeloid cells. Methods Seven patients with XLA with BTK mutations conditioning a null protein expression were included in the study. Monocyte LPS-induced mitogen-activated protein kinase activation, TNF-α and IL-6 production in monocytes, and oxidative burst in monocytes and granulocytes were analyzed by means of flow cytometry. Results We show that in response to LPS, Btk-null monocytes from patients with XLA induce early mitogen-activated protein kinase activation and intracellular TNF-α and IL-6 production with the same intensity as cells from age- and sex-matched control subjects. In addition, the oxidative burst in response to LPS and other stimulants was completely normal in Btk-null monocytes and neutrophils. Conclusion Our results indicate that Btk is not essential for early LPS signaling in human monocytes and that different Btk dependency might exist between human and mouse myeloid cells. Clinical implications These findings provide a better understanding of XLA, and they show the differences between human XLA and murine Xid models.

97 ref.; International audience; Perturbations of the yeast cell wall trigger a repair mechanism that reconfigures its molecular structure to preserve cell integrity. To investigate this mechanism, we compared the global gene expression in five mutant strains, each bearing a mutation (i.e. fks1, kre6, mnn9, gas1, and knr4 mutants) that affects in a different manner the cell wall construction. Altogether, 300 responsive genes were kept based on high stringency criteria during data processing. Functional classification of these differentially expressed genes showed a substantial subset of induced genes involved in cell wall construction and an enrichment of metabolic, energy generation, and cell defense categories, whereas families of genes belonging to transcription, protein synthesis, and cellular growth were underrepresented. Clustering methods isolated a single group of ∼80 up-regulated genes that could be considered as the stereotypical transcriptional response of the cell wall compensatory mechanism. The in silico analysis of the DNA upstream region of these co-regulated genes revealed pairwise combinations of DNA-binding sites for transcriptional factors implicated in stress and heat shock responses (Msn2/4p and Hsf1p) with Rlm1p and Swi4p, two PKC1-regulated transcription factors involved in the activation genes related to cell wall biogenesis and G1/S transition. Moreover, this computational analysis also uncovered the 6-bp 5′-AGCCTC-3′ CDRE (calcineurin-dependent response element) motif in 40% of the co-regulated genes. This motif was recently shown to be the DNA binding site for Crz1p, the major effector of calcineurin-regulated gene expression in yeast. Taken altogether, the data presented here lead to the conclusion that the cell wall compensatory mechanism, as triggered by cell wall mutations, integrates three major regulatory systems: namely the PKC1-SLT2 mitogen-activated protein kinase-signaling module, the “global stress” response mediated by Msn2/4p, and the Ca2+/calcineurin-dependent pathway. The relative importance of these regulatory systems in the cell wall compensatory mechanism is discussed.

The cell wall is an essential structure that preserves the osmotic integrity of fungal cells and determines cellular morphology during developmental programs. The high number of different wall components demands a variety of processes to deliver precursors and synthetic proteins to the proper location at the right time for wall development and modification. Here, the specificity of the mechanisms that regulate the temporal and spatial localisation of cell wall proteins to sites of polarised growth in Saccharomyces cerevisiae is investigated. For this purpose, the localisation of Crh2p, a cell wall glycosylphosphatidylinositol (GPI)-anchored mannoprotein that we have recently described as involved in cell wall construction and localised to polarised growth sites, was followed using a Crh2p-GFP fusion protein. Crh2p distribution was studied in several genetic backgrounds affected in different steps of the cell polarity establishment machinery or/and bud morphogenesis. Crh2p is localised at the mother-bud neck in bud1 cells following the random budding pattern characteristic of this mutant. The Crh2p distribution was greatly altered in a cdc42-1 mutant, indicating complete dependence on an organised actin cytoskeleton for polarised Crh2p distribution. The usual deposition of Crh2p in a ring at the base of growing buds was lacking in cdc10-11 cells growing under restrictive temperature conditions, whereas Crh2p deposition at the septum region was absent in both cdc10-11 and cdc15-lyt1 cells. These results point to the dependence of Crh2p localisation at the bud-neck on both septins and septum integrity. Furthermore, in the absence of Bni4p, a scaffold protein involved in the targeting of the chitin synthase III complex to the bud neck, Crh2p was not longer found at the neck in large-budded cells undergoing cytokinesis. Finally, Crh2p was not properly localised in cells deleted in CHS5 , which encodes a protein involved in the transport of Chs3p, and was completely mislocalised in sbe2/sbe22 mutants, suggesting that the transport systems for Chs3p and Crh2p are to a certain extent coincident. The transport of other GPI-cell wall proteins, such as Cwp1p, however, does not depend on these systems as the localisation of the latter protein was not affected in either of these mutants.