Enhancing MINFLUX 3D imaging precision by vortex interference.

A new acquisition framework for MINFLUX super-resolution microscopy is proposed, termed Vortex Interference MINFLUX (viMINFLUX). From our analysis, we showed that by utilizing vortex interference, the scan range and phase shift mutually modulate MINFLUX precision, resulting in a precision enhancement by a factor of two or more for the same scan range. We further showed that vortex interference can be extended to 3D imaging, whereby 3D viMINFLUX provides for nearly isotropic 3D precision, resulting in a two-fold improvement in lateral precision and a five-fold enhancement in axial precision compared to conventional 3D MINFLUX techniques.

Astrocytes control quiescent NSC reactivation via GPCR signaling-mediated F-actin remodeling.

The transitioning of neural stem cells (NSCs) between quiescent and proliferative states is fundamental for brain development and homeostasis. Defects in NSC reactivation are associated with neurodevelopmental disorders. quiescent NSCs extend an actin-rich primary protrusion toward the neuropil.

Alternative molecular mechanisms for force transmission at adherens junctions via β-catenin-vinculin interaction.

Force transmission through adherens junctions (AJs) is crucial for multicellular organization, wound healing and tissue regeneration. Recent studies shed light on the molecular mechanisms of mechanotransduction at the AJs. However, the canonical model fails to explain force transmission when essential proteins of the mechanotransduction module are mutated or missing.

Astrocytes control quiescent NSC reactivation via GPCR signaling-mediated F-actin remodeling.

The transitioning of neural stem cells (NSCs) between quiescent and proliferative states is fundamental for brain development and homeostasis. Defects in NSC reactivation are associated with neurodevelopmental disorders. quiescent NSCs extend an actin-rich primary protrusion toward the neuropil.

Focal adhesions are controlled by microtubules through local contractility regulation.

Microtubules regulate cell polarity and migration via local activation of focal adhesion turnover, but the mechanism of this process is insufficiently understood. Molecular complexes containing KANK family proteins connect microtubules with talin, the major component of focal adhesions. Here, local optogenetic activation of KANK1-mediated microtubule/talin linkage promoted microtubule targeting to an individual focal adhesion and subsequent withdrawal, resulting in focal adhesion centripetal sliding and rapid disassembly.