Éditeur(s) : HAL CCSD Elsevier
Résumé : International audience
We review the geodynamic evolution of the Aegea-Anatolia region and discuss strain localisation there over geological times. From Late Eocene to Present, crustal deformation in the Aegean backarc has localised progressively during slab retreat. Extension started with the formation of the Rhodope Metamorphic Core Complex (Eocene) and migrated to the Cyclades and the northern Menderes massif (Oligocene and Miocene), accommodated by crustal-scale detachments and a first series of core complexes (MCCs). Extension then localised in Western Turkey, the Corinth Rift and the external Hellenic arc after Messinian times, while the North Anatolian Fault penetrated the Aegean Sea. Through time the direction and style of extension have not changed significantly except in terms of localisation. The contributions of progressive slab retreat and tearing, basal drag, extrusion tectonics and tectonic inheritance are discussed and we favour a model (1) where slab retreat is the main driving engine, (2) successive slab tearing episodes are the main causes of this stepwise strain localisation and (3) the inherited heterogeneity of the crust is a major factor for localising detachments. The continental crust has an inherited strong heterogeneity and crustal-scale contacts such as major thrust planes act as weak zones or as zones of contrast of resistance and viscosity that can localise later deformation. The dynamics of slabs at depth and the asthenospheric flow due to slab retreat also have influence strain localisation in the upper plate. Successive slab ruptures from the Middle Miocene to the Late Miocene have isolated a narrow stripe of lithosphere, still attached to the African lithosphere below Crete. The formation of the North Anatolian Fault is partly a consequence of this evolution. The extrusion of Anatolia and the Aegean extension are partly driven from below (asthenospheric flow) and from above (extrusion of a lid of rigid crust).
ISSN: 0040-1951

insu-00715950
https://hal-insu.archives-ouvertes.fr/insu-00715950
https://hal-insu.archives-ouvertes.fr/insu-00715950/document
https://hal-insu.archives-ouvertes.fr/insu-00715950/file/Jolivet-Aegean_Tectonophysics-2012.pdf
DOI : 10.1016/j.tecto.2012.06.011

Éditeur(s) : HAL CCSD Portland Press
Résumé : International audience
Lutheran (Lu) blood group and Basal Cell Adhesion Molecule (BCAM) antigens both reside on two glycoprotein (gp) isoforms, Lu and Lu(v13), that differ by the size of their cytoplasmic tail. They are receptors of laminin-10/11 and are expressed in red blood cells (RBCs), epithelial cells of multiple tissues and vascular endothelial cells. To gain more insights into the biological function of Lu/BCAM gps, we looked for potential partners of their cytoplasmic tail. We isolated Ubc9 (Ubiquitin-conjugating enzyme 9) protein by screening a human kidney library using the yeast two-hybrid system. Lu/Ubc9 interaction was validated by GST pull-down and co-immunoprecipitation experiments. Endogenous Ubc9 formed a complex with endogenous or recombinant Lu gp in A498 and MDCK epithelial cells, respectively. Substitution of lysine 585 by alanine in the Lu gp, abolished in vitro and ex vivo interaction of Lu gp with Ubc9 protein. Lu K585A mutant transfected in MDCK cells exhibited a normal basolateral membrane expression but was overexpressed at the surface of polarized MDCK cells as compared to wild-type Lu. Pulse-chase experiments showed extended half-life of Lu K585A gp at the plasma membrane, suggesting an impaired endocytosis of this mutant leading to protein accumulation at the membrane. Furthermore, we showed that the ability of MDCK-Lu K585A cells to spread on immobilized laminin was dramatically decreased. Our data supports a physiological role for the direct interaction between Lu gp and Ubc9 protein, and reveals a role for this enzyme in regulating the stability of Lu gp at the cell membrane.
ISSN: 0264-6021

hal-00478614
https://hal.archives-ouvertes.fr/hal-00478614
https://hal.archives-ouvertes.fr/hal-00478614/document
https://hal.archives-ouvertes.fr/hal-00478614/file/PEER_stage2_10.1042%252FBJ20060861.pdf
DOI : 10.1042/BJ20060861