Éditeur(s) : HAL CCSD American Geophysical Union
Résumé : International audience
Detection and attribution of human influence on sea level rise are important topics that have not yet been explored in depth. We question whether the sea level changes (SLC) over the past century were natural in origin. SLC exhibit power law long-term correlations. By estimating Hurst exponent through Detrended Fluctuation Analysis and by applying statistics of Lennartz and Bunde [2009], we search the lower bounds of statistically significant external sea level trends in longest tidal records worldwide. We provide statistical evidences that the observed SLC, at global and regional scales, is beyond its natural internal variability. The minimum anthropogenic sea level trend (MASLT) contributes to the observed sea level rise more than 50% in New York, Baltimore, San Diego, Marseille, and Mumbai. A MASLT is about 1 mm/yr in global sea level reconstructions that is more than half of the total observed sea level trend during the XXth century.
ISSN: 0094-8276

hal-01336190
https://hal.archives-ouvertes.fr/hal-01336190
https://hal.archives-ouvertes.fr/hal-01336190/document
https://hal.archives-ouvertes.fr/hal-01336190/file/BECKER2014a.pdf
DOI : 10.1002/2014GL061027

Éditeur(s) : HAL CCSD Nature Publishing Group
Résumé : International audience
CYLD is a tumour suppressor gene mutated in familial cylindromatosis, a genetic disorder leading to the development of skin appendage tumours. It encodes a deubiquitinating enzyme that removes Lys63- or linear-linked ubiquitin chains. CYLD was shown to regulate cell proliferation, cell survival and inflammatory responses, through various signalling pathways. Here we show that CYLD localizes at centrosomes and basal bodies via interaction with the centrosomal protein CAP350 and demonstrate that CYLD must be both at the centrosome and catalytically active to promote ciliogenesis independently of NF-κB. In transgenic mice engineered to mimic the smallest truncation found in cylindromatosis patients, CYLD interaction with CAP350 is lost disrupting CYLD centrosome localization, which results in cilia formation defects due to impairment of basal body migration and docking. These results point to an undiscovered regulation of ciliogenesis by Lys63 ubiquitination and provide new perspectives regarding CYLD function that should be considered in the context of cylindromatosis.
ISSN: 2041-1723

hal-01063915
https://hal.archives-ouvertes.fr/hal-01063915
DOI : 10.1038/ncomms5585
PUBMED : 25134987