Granular flow in polymineralic rocks bearing sheet silicates: New evidence from natural examples

Natural deformation in carbonate mylonites bearing sheet silicates occurs via a complex interaction of granular flow and solution transfer processes and involves continuous cycles of dissolution, grain boundary diffusion, nucleation and growth. In this way, new sheet silicates (a) nucleate within voids formed by grain boundary sliding of calcite grains. (b) grow, and (c) rotate towards the shear plane. As a consequence, small mica grains show a wide range of orientations with respect to the shear plane, but moderate to large grains are subparallel both to each other and to the shear plane. Increases of average grain sizes with increasing temperature of sheet silicates in mica-rich layers is more pronounced than in mica-poor layers. In the calcitic matrix however, sheet silicates can only grow via solution-precipitation and mass transfer processes. Therefore, the observed grain size variability indicates drastic differences in mass transfer behavior between the individual layers, which might be related to differences in the fluid flux. Based on these observations, a conceptual model for the microfabric evolution in sheet silicate bearing mylonites is presented. © 2001 Elsevier Science B.V. All rights reserved.

FOXC2 and fluid shear stress stabilize postnatal lymphatic vasculature

Biomechanical forces, such as fluid shear stress, govern multiple aspects of endothelial cell biology. In blood vessels, disturbed flow is associated with vascular diseases, such as atherosclerosis, and promotes endothelial cell proliferation and apoptosis. Here, we identified an important role for disturbed flow in lymphatic vessels, in which it cooperates with the transcription factor FOXC2 to ensure lifelong stability of the lymphatic vasculature. In cultured lymphatic endothelial cells, FOXC2 inactivation conferred abnormal shear stress sensing, promoting junction disassembly and entry into the cell cycle. Loss of FOXC2-dependent quiescence was mediated by the Hippo pathway transcriptional coactivator TAZ and, ultimately, led to cell death. In murine models, inducible deletion of Foxc2 within the lymphatic vasculature led to cell-cell junction defects, regression of valves, and focal vascular lumen collapse, which triggered generalized lymphatic vascular dysfunction and lethality. Together, our work describes a fundamental mechanism by which FOXC2 and oscillatory shear stress maintain lymphatic endothelial cell quiescence through intercellular junction and cytoskeleton stabilization and provides an essential link between biomechanical forces and endothelial cell identity that is necessary for postnatal vessel homeostasis. As FOXC2 is mutated in lymphedema-distichiasis syndrome, our data also underscore the role of impaired mechanotransduction in the pathology of this hereditary human disease.