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The downscaling of optical systems to the micro and nano-scale results in very compliant systems with nanogram-scale masses, which renders them susceptible to optical forces. Here we show a specially designed resonant structure for enabling efficient static control of the optical response with relatively weak repulsive and attractive optical forces. Using attractive gradient optical forces we demonstrate a static mechanical deformation of up to 20 nanometers in the resonator structure.

Cell growth and differentiation are critically dependent upon matrix rigidity, yet many aspects of the cellular rigidity-sensing mechanism are not understood. Here, we analyze matrix forces after initial cell-matrix contact, when early rigidity-sensing events occur, using a series of elastomeric pillar arrays with dimensions extending to the submicron scale (2, 1, and 0.5 μm in diameter covering a range of stiffnesses). We observe that the cellular response is fundamentally different on micron-scale and submicron pillars. On 2-μm diameter pillars, adhesions form at the pillar periphery, forces are directed toward the center of the cell, and a constant maximum force is applied independent of stiffness. On 0.5-μm diameter pillars, adhesions form on the pillar tops, and local contractions between neighboring pillars are observed with a maximum displacement of ∼60 nm, independent of stiffness. Because mutants in rigidity sensing show no detectable displacement on 0.5-μm diameter pillars, there is a correlation between local contractions to 60 nm and rigidity sensing. Localization of myosin between submicron pillars demonstrates that submicron scale myosin filaments can cause these local contractions. Finally, submicron pillars can capture many details of cellular force generation that are missed on larger pillars and more closely mimic continuous surfaces.cell mechanics | mechanotransduction | nanofabrication T he rigidity of matrix substrates provides important signals that determine cell growth (1), differentiation (2, 3), adhesion (4), or motility (5), among others. How the cellular motility machinery can sense matrix rigidity is unknown, but the mechanism(s) of rigidity sensing must be constrained by the size of the rigidity sensing machinery and the physical quantity "measured" by the cell (6). Arrays of elastomeric micropillars have proven to be a valuable tool in measuring cellular forces: optical microscopy can be used to precisely measure pillar displacement and generate real-time force maps across entire cells (7, 8). For example, over the time scale of hours to days, fibroblasts on arrays of 1-and 2-μm diameter pillars generate average displacements on the order of 100 nm independent of the pillar stiffness over a range of 2-130 nN/μm, i.e., the cells respond to rigidity by measuring the force required to produce a constant displacement (9). However, no studies have examined forces during the initial contact between the cell and the substrate, when the first rigiditysensing events take place (10). Moreover, in studies of the minimal cell-substrate contact area needed to sense rigidity and assemble adhesions, fibroblasts assembled adhesion contacts at the edges of beads with contact areas of more than ∼1 μm 2 , whereas with submicron beads, adhesion contacts only assembled after force from a rigid laser tweezers was applied (11). Analysis of bead displacement with laser tweezers also suggests that cells measure the force required for local displacements of ∼100 nm to deduce rigidity, i.e., a constant displ...

Mechanical forces have key roles in regulating activation of T cells and coordination of the adaptive immune response. A recent example is the ability of T cells to sense the rigidity of an underlying substrate through the T-cell receptor (TCR) coreceptor CD3 and CD28, a costimulation signal essential for cell activation. In this report, we show that these two receptor systems provide complementary functions in regulating the cellular forces needed to test the mechanical properties of the extracellular environment. Traction force microscopy was carried out on primary human cells interacting with micrometer-scale elastomer pillar arrays presenting activation antibodies to CD3 and/or CD28. T cells generated traction forces of 100 pN on arrays with both antibodies. By providing one antibody or the other in solution instead of on the pillars, we show that force generation is associated with CD3 and the TCR complex. Engagement of CD28 increases traction forces associated with CD3 through the signaling pathway involving PI3K, rather than providing additional coupling between the cell and surface. Force generation is concentrated to the cell periphery and associated with molecular complexes containing phosphorylated Pyk2, suggesting that T cells use processes that share features with integrin signaling in force generation. Finally, the ability of T cells to apply forces through the TCR itself, rather than the CD3 coreceptor, was tested. Mouse cells expressing the 5C.C7 TCR exerted traction forces on pillars presenting peptide-loaded MHCs that were similar to those with α-CD3, suggesting that forces are applied to antigen-presenting cells during activation.T -cell activation is a key regulatory point of the adaptive immune response. It is initiated by recognition of peptideloaded MHCs (pMHCs) on antigen-presenting cells (APCs) by T-cell receptors (TCRs). Engagement of additional receptors on the T-cell surface leads to formation of a specialized interface termed the immune synapse (IS), which focuses communication between these cells. The IS has emerged as a compelling model of juxtacrine signaling, providing key insights into how the dynamics of such interfaces influence cell-cell communication. Mechanical forces originating from a range of sources, including cytoskeletal dynamics, also play important roles in T-cell activation. The initial spreading of T cells following contact with an activating surface is dependent on a burst of actin polymerization (1, 2). Subsequent retrograde flow of actin and contraction of actomyosin structures drive microscale reorganization of signaling complexes within this interface, resulting in formation of concentric central, peripheral, and distal supramolecular activation cluster (cSMAC, pSMAC, and dSMAC) structures that comprise the archetypal IS (3-8). The TCR complex itself may be triggered by external forces (9, 10), whereas TCR ligation may induce actin polymerization and generation of protrusive forces (11).More recently, mechanosensing by T cells was demonstrated in the context ...

We demonstrate high confinement, low-loss silicon nitride ring resonators with intrinsic quality factor (Q) of 3*10(6) operating in the telecommunication C-band. We measure the scattering and absorption losses to be below 0.065dB/cm and 0.055dB/cm, respectively.