Small-scale soft continuum robots capable of active steering and navigation in a remotely controllable manner hold great promise in diverse areas, particularly in medical applications. Existing continuum robots, however, are often limited to millimeter or centimeter scales due to miniaturization challenges inherent in conventional actuation mechanisms, such as pulling mechanical wires, inflating pneumatic or hydraulic chambers, or embedding rigid magnets for manipulation. In addition, the friction experienced by the continuum robots during navigation poses another challenge for their applications. Here, we present a submillimeter-scale, self-lubricating soft continuum robot with omnidirectional steering and navigating capabilities based on magnetic actuation, which are enabled by programming ferromagnetic domains in its soft body while growing hydrogel skin on its surface. The robot’s body, composed of a homogeneous continuum of a soft polymer matrix with uniformly dispersed ferromagnetic microparticles, can be miniaturized below a few hundreds of micrometers in diameter, and the hydrogel skin reduces the friction by more than 10 times. We demonstrate the capability of navigating through complex and constrained environments, such as a tortuous cerebrovascular phantom with multiple aneurysms. We further demonstrate additional functionalities, such as steerable laser delivery through a functional core incorporated in the robot’s body. Given their compact, self-contained actuation and intuitive manipulation, our ferromagnetic soft continuum robots may open avenues to minimally invasive robotic surgery for previously inaccessible lesions, thereby addressing challenges and unmet needs in healthcare.

The Hippo pathway senses cellular conditions and regulates YAP/TAZ to control cellular and tissue homeostasis, while TBK1 is central for cytosolic nucleic acid sensing and antiviral defense. The correlation between cellular nutrient/physical status and host antiviral defense is interesting but not well understood. Here we find that YAP/TAZ act as natural inhibitors of TBK1 and are vital for antiviral physiology. Independent of transcriptional regulation and through transactivation domain, YAP/TAZ associate directly with TBK1 and abolish virus-induced TBK1 activation, by preventing TBK1 K63-linked ubiquitination and adaptors/substrates binding. Accordingly, YAP/TAZ deletion/depletion or cellular conditions inactivating YAP/TAZ through Lats1/2 kinases relieve TBK1 suppression and boost antiviral responses, whereas expression of the transcriptionally inactive YAP dampens cytosolic RNA/DNA sensing and weakens the antiviral defense in cells and zebrafish. Thus, we describe a function of YAP/TAZ and the Hippo pathway in innate immunity, by linking cellular nutrient/physical status to antiviral host defense.

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