Self-sensing cellulose structures with design-controlled stiffness

Robots are often used for sensing and sampling in natural environments. Within this area, soft robots have become increasingly popular for these tasks because their mechanical compliance makes them safer to interact with. Unfortunately, if these robots break while working in vulnerable environments, they create potentially hazardous waste. Consequently, the development of compliant, biodegradable structures for soft, eco-robots is a relevant research area that we explore here. Cellulose is one of the most abundant biodegradable materials on earth, but it is naturally very stiff, which makes it difficult to use in soft robots. Here, we look at both biologically and kirigami inspired structures that can be used to reduce the stiffness of cellulose based parts for soft robots up to a factor of 19 000. To demonstrate this, we build a compliant force and displacement sensing structure from microfibrillated cellulose. We also describe a novel manufacturing technique for these structures, provide mechanical models that allow designers to specify their stiffness, and conclude with a description of our structure's performance

Molecular basis of ClC-6 function and its impairment in human disease

ClC-6 is a late endosomal voltage-gated chloride-proton exchanger that is predominantly expressed in the nervous system. Mutated forms of ClC-6 are associated with severe neurological disease. However, the mechanistic role of ClC-6 in normal and pathological states remains largely unknown. Here, we present cryo-EM structures of ClC-6 that guided subsequent functional studies. Previously unrecognized ATP binding to cytosolic ClC-6 domains enhanced ion transport activity. Guided by a disease-causing mutation (p.Y553C), we identified an interaction network formed by Y553/F317/T520 as potential hotspot for disease-causing mutations. This was validated by the identification of a patient with a de novo pathogenic variant p.T520A. Extending these findings, we found contacts between intramembrane helices and connecting loops that modulate the voltage dependence of ClC-6 gating and constitute additional candidate regions for disease-associated gain-of-function mutations. Besides providing insights into the structure, function, and regulation of ClC-6, our work correctly predicts hotspots for CLCN6 mutations in neurodegenerative disorders