1,721,205 research outputs found

    Preface

    No full text

    Meiotic double strand breaks repair in sexually reproducing eukaryotes: We are not all equal.

    Full text link
    The defining event of meiosis is prophase-I, during which the maternal and paternal chromosome find each other in the nucleus, pair, and align in a process called “synapses of the homologues”. Their faithful segregation during the first meiotic division (MI) requires meiotic recombination and in particular at least one crossing over (CO) per pair of homologous chromosomes. COs are needed, not only to generate diversity within a population, but (along with sister chromatids cohesion) to form the chiasmata that are the physical connection between the homologues that ensures their faithful segregation at metaphase-I. Our understanding of recombination in higher eukaryotes has comes from studies in model organisms such as yeasts, flies and worms. Although there are clear differences among organisms, most of the genes and proteins that are required in these processes are conserved and have orthologues in mammals. However, their null mutations in mice (Mus musculus) do not always display the same phenotype as in lower eukaryotes, indicating that along with the increased complexity of the genome, same genes have acquired new or partially overlapping functions. In this review we will focus on the main genes and protein products which are required for meiotic recombination, comparing the simple metazoan C. elegans and the mouse, underlying divergences and similarities between these organism

    Seismicity of central Italy in the context of the geological history of the Umbria-Marche Apennines

    No full text
    In the Umbria-Marche Apennines, direct evidence of earthquakes (including data from geodetic, geophysical, historical, and paleoseismological research) is not older than 20–10 ka, but the events themselves are influenced by the whole ~250 m.y. geo- logical history of the region. For seismic sequences that have occurred in the past few decades, seismological data of increasing quality provide detailed images of the active NNW-SSE–trending normal fault systems in the upper 10 km of the crust. Major historical earthquakes and sparse paleoseismological data are also aligned parallel to the same lineaments, which clearly define the distribution of the major seismogenic sources of the region. The close connection between active tectonics and older Quater- nary faults that border a series of extensional intramountain basins is demonstrated by the fact that seismogenic and Quaternary faults are distributed along the same alignments, formed within similarly oriented stress fields, and accommodate WSW- ENE extension coherently with the active strain field. The Quaternary to present tec- tonics form part of a long-lived extensional process, active over 15–20 m.y., which is migrating eastward through time across the Italian peninsula, superimposed on the previous compressional phase that created the Apennines. The older Umbria-Marche geological history, recorded in the Triassic to Paleogene stratigraphic succession of the region, also influences the present-day distribution of seismicity. Specifically, the complex mechanical stratigraphy of the region determines the superposition of rocks with different rheological behaviors and overall thickness of the seismogenic layer. Almost all of the earthquakes occur within the sedimentary cover, with main shocks located close to the basal contact with the underlying Paleozoic basement

    Il paesaggio geologico della Valnerina

    No full text
    Descrizione del paesaggio fisico della Valnerin

    Seeking new meiotic genes

    Full text link

    Revisiting DNA damage repair, p53-mediated apoptosis and cisplatin sensitivity in germ cell tumors

    Full text link
    Testicular germ cell tumors (TGCTs), ie, seminomas and nonseminomas, account for 1% to 3% of all neoplasms in men. They are the most common cancer in young white males and are unique in their responsiveness to cisplatin-based chemotherapy. For this reason, TGCTs are considered a model for curative disease. However, up to now, the molecular mechanisms behind this exceptional responsiveness to DNA-damaging agents have remained unclear. A hypersensitive apoptotic response, as well as a reduction in the proficiency to repair cisplatin-induced DNA damage might account for this behavior. In this review, building on recent findings of p53-induced apoptosis and DNA-repair mechanisms in TGCTs, we will discuss the molecular bases that drive tumor sensitivity to cisplatin, emphasizing the new therapeutic approaches proposed to eventually constrain tumor recurrence, and target TGCTs which are unresponsive to standard therapies
    corecore