A5007077666- RNA Research and Splicing
- Autophagy in Disease and Therapy
- RNA modifications and cancer
- CRISPR and Genetic Engineering
- S100 Proteins and Annexins
- Barrier Structure and Function Studies
- Cell Adhesion Molecules Research
- Cancer-related gene regulation
- Cellular Mechanics and Interactions
- Chemical Synthesis and Analysis
- Pancreatic function and diabetes
- Nuclear Structure and Function
- Heat shock proteins research
- Calcium signaling and nucleotide metabolism
- Neuroscience and Neuropharmacology Research
- Cellular transport and secretion
- Lipid metabolism and biosynthesis
- Tissue Engineering and Regenerative Medicine
- Hippo pathway signaling and YAP/TAZ
- Adenosine and Purinergic Signaling
- Wnt/β-catenin signaling in development and cancer
- RNA Interference and Gene Delivery
- Alzheimer's disease research and treatments
- RNA and protein synthesis mechanisms
- Cancer Cells and Metastasis
Max Planck Institute of Molecular Cell Biology and Genetics
2021-2025
Center for Systems Biology Dresden
2025
Technische Universität Dresden
2024-2025
Tsinghua University
2014-2023
Peking University
2014-2022
Center for Life Sciences
2014-2022
Misfolded proteins can be degraded by selective autophagy. The prevailing view is that ubiquitin-tagged misfolded are assembled into aggregates the scaffold protein p62, and then engulfed autophagosomes. Here we report p62 forms droplets in vivo which have liquid-like properties such as high sphericity, ability to undergo fusion, recovery after photobleaching. Recombinant does not phase separation vitro; however, adding a K63 polyubiquitin chain induces separation, results enrichment of...
Organisms have evolved elaborate mechanisms to adjust intracellular nutrient levels in response fluctuating availability of exogenous nutrients. During starvation, cells can enhance amino acid uptake and synthesis through the general control (GAAC) pathway, whereas nonessential cellular contents are recycled by autophagy. How these two pathways coordinated starvation is currently unknown. Here we show that GAAC pathway couples with Starvation caused deactivation mTOR, which then activated In...
Abstract Autophagosomes are double-membrane vesicles generated intracellularly to encapsulate substrates for lysosomal degradation during autophagy. Phase separated p62 body plays pivotal roles autophagosome formation, however, the underlying mechanisms still not fully understood. Here we describe a spatial membrane gathering mode by which functions in formation. Mass spectrometry-based proteomics reveals significant enrichment of vesicle trafficking components within body. Combining...
Alzheimer's disease begins with mild memory loss and slowly destroys thinking. Cognitive impairment in has been associated the localization of microtubule-associated protein Tau at postsynapse. However, correlation between postsynapse synaptic dysfunction remains unclear. Here, we show that arrests liquid-like droplets formed by four postsynaptic density proteins PSD-95, GKAP, Shank, Homer solution, as well NMDA (N-methyl-D-aspartate)-receptor-associated clusters on synthetic membranes....
Tight junctions play an essential role in sealing tissues, by forming belts of adhesion strands around cellular perimeters. Recent work has shown that the condensation ZO1 scaffold proteins is required for tight junction assembly. However, mechanisms which junctional condensates initiate at cell-cell contacts and elongate cell perimeters remain unknown. Combining biochemical reconstitutions live-cell imaging MDCKII tissue, we found belt formation driven receptor-mediated surface coupled to...
A key mediator of macroautophagy/autophagy induction is the class III phosphatidylinositol 3-kinase complex I (PtdIns3K-C1) consisting PIK3C3/VPS34, PIK3R4/VPS15, BECN1, and ATG14. Although several proteins are known to enhance or decrease PtdIns3K-C1 activity, our understanding molecular regulation still incomplete. Previously, we identified a Golgi-associated protein, GLIPR2, in screen for that interact with amino acids 267-284 region BECN1 sufficient induce autophagy when fused cell...
Surface binding and surface phase separation of cytosolic scaffold proteins on lipid membranes are involved in many cellular processes such as cell signaling, adhesion, cortex regulation. However, the interplay between is poorly understood. In this work, we study by deriving a general thermodynamic model applying it to vitro reconstitution experiments membrane-binding tight junction initiation. Our theory extends classical isotherm account for non-dilute heterogeneous conditions where...
Epithelial morphogenesis relies on coordinated multicellular movements regulated by adhesion and force-generating molecules. It remains elusive how cells ensure organization of these molecules in space time. Combining vitro reconstitution fly genetics, we demonstrate that condensation an adhesive transmembrane protein shapes molecular dynamics at tricellular junctions to facilitate cell-cell junction remodeling. Specifically, identify the intracellular domain Sidekick, known localize recruit...
Liquid-liquid phase separation (LLPS) underlies the formation mechanism of membraneless biomolecular condensates locally to perform important physiological functions such as selective autophagy, but little is known about relationship between their dynamic structural organization and biophysical properties. Here, a dark-field microscopy based single plasmonic nanoparticle tracking (DFSPT) technique was introduced simultaneously monitor diffusion dynamics multiple gold nanorod (AuNR) probes in...
Abstract Formation of biomolecular condensates via phase separation enables compartmentation many cellular processes. However, how cells can control condensation at specific locations to create complex structures remains poorly understood. Here, we investigated the mechanism tight junction formation, which involves scaffold proteins cell-cell contacts and elongation into a belt around perimeter. Using cell biology, reconstitution, thermodynamic theory, discovered that use surface transitions...
C-terminal alpha 1-antitrypsin peptides induce tight junction formation by activating G protein G13.
Tight junctions play an essential role in sealing tissues, by forming belts of adhesion strands around cellular perimeters. The formation a tight junction occurs into two steps, initiation at cell-cell contacts, and elongation the perimeter. Recent work has shown that nucleation is governed condensation scaffold proteins. However, mechanisms which condensates are spatially controlled to initiate contacts elongate cell perimeters remain unknown. Here, we combined biology, molecular...
Abstract Tight junctions play an essential role in sealing tissues, by forming belts of adhesion strands around cellular perimeters. The formation a tight junction occurs into two steps, initiation at cell-cell contacts, and elongation the perimeter. Recent work has shown that nucleation is governed condensation scaffold proteins. However, mechanisms which condensates are spatially controlled to initiate contacts elongate cell perimeters remain unknown. Here, we combined biology, molecular...