7 research outputs found

    Strengths and weaknesses of Primary Healthcare staff to design multidisciplinary or interdisciplinary strategies of physical activity on prescription in Madrid Healthcare System

    No full text
    Physical inactivity and sedentary levels currently represent one of the major threats to public health. Physical activity on prescription (PAP) is an emerging preventive and treatment resource for non-communicable chronic diseases in healthcare settings. The aim of this study was to analyze the feasibility of implementing PAP at Primary Healthcare (PHC) centres in the Region of Madrid

    The Anaphase Promoting Complex Targeting Subunit Ama1 Links Meiotic Exit to Cytokinesis during Sporulation in Saccharomyces cerevisiae

    No full text
    Ascospore formation in yeast is accomplished through a cell division in which daughter nuclei are engulfed by newly formed plasma membranes, termed prospore membranes. Closure of the prospore membrane must be coordinated with the end of meiosis II to ensure proper cell division. AMA1 encodes a meiosis-specific activator of the anaphase promoting complex (APC). The activity of APCAma1 is inhibited before meiosis II, but the substrates specifically targeted for degradation by Ama1 at the end of meiosis are unknown. We show here that ama1Δ mutants are defective in prospore membrane closure. Ssp1, a protein found at the leading edge of the prospore membrane, is stabilized in ama1Δ mutants. Inactivation of a conditional form of Ssp1 can partially rescue the sporulation defect of the ama1Δ mutant, indicating that an essential function of Ama1 is to lead to the removal of Ssp1. Depletion of Cdc15 causes a defect in meiotic exit. We find that prospore membrane closure is also defective in Cdc15 and that this defect can be overcome by expression of a form of Ama1 in which multiple consensus cyclin-dependent kinase phosphorylation sites have been mutated. These results demonstrate that APCAma1 functions to coordinate the exit from meiosis II with cytokinesis

    Glucanases and Chitinases

    No full text
    In many yeast and fungi, β-(1,3)-glucan and chitin are essential components of the cell wall, an important structure that surrounds cells and which is responsible for their mechanical protection and necessary for maintaining the cellular shape. In addition, the cell wall is a dynamic structure that needs to be remodelled along with the different phases of the fungal life cycle or in response to extracellular stimuli. Since β-(1,3)-glucan and chitin perform a central structural role in the assembly of the cell wall, it has been postulated that β-(1,3)-glucanases and chitinases should perform an important function in cell wall softening and remodelling. This review focusses on fungal glucanases and chitinases and their role during fungal morphogenesis.This work was supported by grants from the Spanish Government to CR (BFU2017-84508-P) and CRV (BIO2015-70195-C2-1-R) and from Junta de Castilla y León to CR (SA116G19). The IBFG is supported by Programa “Escalera de Excelencia” from Junta de Castilla y León (CLU-2017-03) and University of Salamanca. All Spanish funding is co-sponsored by the European Union FEDER programme.Peer reviewe

    Heritable epigenetic mutation of a transposon-flanked Arabidopsis gene due to lack of the chromatin-remodeling factor DDM1

    No full text
    Epigenetically silent transposons and repeats constitute a substantial proportion of eukaryotic genomes, but their impact on cellular gene function remains largely unexplored. In Arabidopsis, transposons are silenced by DNA methylation, and this methylation is often abolished by mutations in a chromatin-remodeling gene DDM1 (DECREASE IN DNA METHYLATION 1). The ddm1 mutation induces various types of developmental abnormalities through de-repression of transposons and repeats. Here, we report a novel mechanism for a ddm1-induced syndrome, called bonsai (bns). We identified the gene responsible for the bns phenotypes by genetic linkage analysis and subsequent transcriptional analysis. The bns phenotypes are due to silencing of a putative Anaphase-Promoting Complex (APC) 13 gene. The BNS gene silencing was associated with DNA hypermethylation, which is in contrast to the ddm1-induced hypomethylation in the other genomic regions. This paradoxical BNS hypermethylation was reproducibly induced during self-pollination of the ddm1 mutant, and it was mediated by a long interspersed nuclear element (LINE) retrotransposon flanking the BNS gene. We discuss possible molecular mechanisms and the evolutionary implications of transposon-mediated epigenetic changes in the BNS locus
    corecore