No abstract

Until now, the green and facile synthesis of highly fluorescent silicon nanoparticles (SiNPs) with robust luminescent stability and favorable biocompatibility for cellular imaging is still a challenge. Here, a novel biomimetic strategy is demonstrated for the preparation of cell-tailored fluorescent SiNPs by the effective reaction of the easily available and operable yeast secretion and silicon precursor, K2SiF6. The as-prepared SiNPs exhibit excellent water dispersibility, favorable biocompatibility, and high luminescence (photoluminescent quantum yield of 44.77%) with robust pH/photo-/storage stability, holding great promise for use as new-generation fluorescent probes for long-term cellular imaging. Notably, it is found that several yeast-derived proteins, as reductants and stabilizers, played constructive roles in the fabrication of SiNPs with such inherent unique properties. The abundant amino and carboxyl groups could not only stabilize the resultant SiNPs with excellent water dispersibility but also functionalize them for further biomedical and biological applications. The biomimetic route has broken through the bottleneck hit by current physical or chemical methods in the green synthesis of SiNPs and provided a prospective direction for future nanotechnology.

Synthetic signalling receptors enable programmable cellular responses coupling with a customized input. However, engineering a designer force-sensing receptor to rewire mechanotransduction remains largely unexplored. Herein, we introduce nongenetically engineered artificial mechanoreceptors (AMRs) capable of reprogramming non-mechanoresponsive receptor tyrosine kinases (RTKs) to sense user-defined force cues, enabling a de novo designed mechanotransduction. AMR is a modular DNA-protein chimera comprising a mechanosensing-and-transmitting DNA nanodevice grafted on natural RTKs via aptameric anchors. AMR senses intercellular tensile force via an allosteric DNA mechano-switch with tuneable piconewton-sensitive force tolerance, actuating a force-triggered dynamic DNA assembly to manipulate RTK dimerization and activate intracellular signalling. By swapping the force-reception ligands, we demonstrate the AMR-mediated activation of c-Met, a representative RTK, in response to the cellular tensile forces mediated by cell-adhesion proteins (integrin, E-cadherin) or membrane protein endocytosis (CI-M6PR). Moreover, the versatility of AMR allows the reprogramming of FGFR1, another RTK, to customize mechanobiological function, e.g., adhesion-mediated neural stem cell maintenance.