After a successful year of group meetings organized by technology and focused on learning one another’s skills and interests, the CEMB has restructured for its second year. This restructuring, agreed upon unanimously at the 2017 annual retreat, will enable us to harness these skills to address the most pressing questions in mechanobiology. The proposed questions and the new organizational structure associated with them are presented below.
Question 1: How do cells sense their mechanical environment?
Liz Haswell (WashU) and E. Michael Ostap (Penn)
(1) Mechanisms and molecular components of viscoelastic sensing
What aspects of adhesions, plasmodesmata connections, filopodial dynamics, and cytoskeletal dynamics contribute?
(2) Mechanosensing across proteins, supramolecular structures and organelles
How do the Golgi apparatus, ER, vacuole, cytoskeleton, proteoglycan/arabinogalactan structures, and nuclear deformation contribute?
Question 2: How do cells adapt to and change their mechanical environment?
Ram Dixit (WashU) and Paul Janmey (Penn)
(1) Recursive feedback between cells and the wall/ECM
How do changes to the adhesions, cytoskeleton, vacuole, nucleus, and ECM/wall microenvironment of a cell affect one another?
(2) Interaction between stress and soluble factors
How do soluble factors arise from mechanical stimulus, and how do these change the biomechanics of recursive feedback between the cell and the wall/ECM?
Question 3: How do cells remember their mechanical environment?
Rob Mauck (Penn) and Lucia Strader (WashU)
1) Cytoskeletal, microenvironmental plasticity, and ECM plasticity
How does emerging information about the inelastic and time-varying deformation of the cell microenvironment change our elasticity-based understanding of mechanobiology?
(2) Nuclear plasticity, mechanochemistry and epigenetics
Do severe changes to the shape of the nucleus and nuclear envelope change DNA expression over meaningful periods of time? What governs this plasticity?
Under what circumstances can mechanical force lead to chemical changes that lock in changes to gene expression (due to LADS, methylation, and acetylation) permanently in a cell and its descendants?
Group 4: Crosscutting and Emerging Technologies Working Group
Chris Chen (BU) and Derrick Dean (ASU)
(1) Biomimetic platforms and standardized models for tissue remodeling, morphogenesis and development
Including fibrosis-on a chip and plant-on-a-chip
Refined in vivo animal and plant models
(2) Engineered force sensors and stress channels
Tailored ion channels and molecular beacons including nesprin sensors