Whole chromosome aneuploidy in the brain of Bub1bH/H and Ercc1-/Δ7 mice

High levels of aneuploidy have been observed in disease-free tissues, including post-mitotic tissues such as the brain. Using a quantitative interphase-fluorescence in situ hybridization approach, we previously reported a chromosome-specific, age-related increase in aneuploidy in the mouse cerebral cortex. Increased aneuploidy has been associated with defects in DNA repair and the spindle assembly checkpoint, which in turn can lead to premature aging. Here, we quantified the frequency of aneuploidy of three autosomes in the cerebral cortex and cerebellum of adult and developing brain of Bub1b(H/H) mice, which have a faulty mitotic checkpoint, and Ercc1(-/Δ7) mice, defective in nucleotide excision repair and inter-strand cross-link repair. Surprisingly, the level of aneuploidy in the brain of these murine models of accelerated aging remains as low as in the young adult brains from control animals, i.e. <1% in the cerebral cortex and ∼0.1% in the cerebellum. Therefore, based on aneuploidy, these adult mice with reduced life span and accelerated progeroid features are indistinguishable from age-matched, normal controls. Yet, during embryonic development, we found that Bub1b(H/H), but not Ercc1(-/Δ7) mice, have a significantly higher frequency of aneuploid nuclei relative to wild-type controls in the cerebral cortex, reaching a frequency as high as 40.3% for each chromosome tested. Aneuploid cells in these mutant mice are likely eliminated early in development through apoptosis and/or immune-mediated clearance mechanisms, which would explain the low levels of aneuploidy during adulthood in the cerebral cortex of Bub1b(H/H) mice. These results shed light on the mechanisms of removal of aneuploidy cells in vivo

Staphylococcus lugdunensis, an aggressive coagulase-negative pathogen not to be underestimated

The new emerging coagulase-negative pathogen Staphylococcus lugdunensis is responsible for severe cardiac and joint infections. Since the biochemical phenotypic systems designed for the identification of CoNS do not appear to be species specific and are hardly reliable for the discrimination of S. lugdunensis from other staphylococci, its precise identification requires fine molecular methods. The pathogenic mechanisms by which S. lugdunensis causes severe infections are not yet completely elucidated and in this review its virulence and toxic determinants are surveyed as well as its adhesins and biofilm production