Projekt

Life is a homeostatic microenvironment, defined in all extant life forms by a fluid lipid membrane that separates life from non-life. This membrane is not a passive barrier, but also constitutes the functional interface between life and its surroundings, which must adaptively respond to life's homeostatic demands. In living membranes, homeostasis is under constant challenge from physical and biochemical stressors, with dysfunctional responses leading to adverse outcomes. Despite the fundamental role of responsive membranes in defining and sustaining life, there is remarkably little understanding of the mechanisms by which cells sense and respond to changes in membrane properties. This project aims to define these sense-and-respond mechanisms from molecules to organisms across the tree of life, from the simplest living organism to multicellular animals. Converging insights across systems will define the basic principles of membrane homeostasis toward the goal of understanding, and extending, life. The ultimate vision of this work is a synthetic, responsive, self-maintaining, and growing membrane that will comprise an essential part of the first synthetic cell.

• Prof. Dr. Robert Ernst

  Universitätsklinikum des Saarlandes
  Institut für Biochemie
  Homburg
  

• Dr. James Saenz, Ph.D.

  Technische Universität Dresden
  B Cube - Center for Molecular Bioengineering
  Laboratory of Synthetic Membrane Biology
  Dresden
  

• Prof. Ilya Levental, Ph.D.

  University of Virginia
  Center for Membrane and Cell Physiology
  Molecular Physiology and Biological Physics
  Levental Laboratory of Membrane Biology
  Pinn Hall Room 4011
  Charlottesville
  USA
  

• Prof. Maya Schuldiner, Ph.D.

  The Weizmann Institute of Science
  Department of Molecular Genetics
  Biochemistry
  Rehovot
  Israel
  

• Lipidomic and biophysical homeostasis of mammalian membranes counteracts dietary lipid perturbations to maintain cellular fitness

• Regulation of lipid saturation without sensing membrane fluidity

• Principles of membrane adaptation revealed through environmentally induced bacterial lipidome remodeling.

• Iron affects Ire1 clustering propensity and the amplitude of endoplasmic reticulum stress signaling