Search bioRxiv⌕ Search
Home/Archive/bioRxiv

bioRxiv · 10.1101/2019.12.30.881557

Protein-free division of giant unilamellar vesicles controlled by enzymatic activity

Dreher, Y.·Spatz, J. P.·Göpfrich, K.
View original source ↗Export metadata ↓

Abstract

Cell division is one of the hallmarks of life. Success in the bottom-up assembly of synthetic cells will, no doubt, depend on strategies for the controlled autonomous division of protocellular compartments. Here, we describe the protein-free division of giant unilamellar lipid vesicles (GUVs) based on the combination of two physical principles - phase separation and osmosis. We visualize the division process with confocal fluorescence microscopy and derive a conceptual model based on the vesicle geometry. The model successfully predicts the shape transformations over time as well as the time point of the final pinching of the daughter vesicles. Remarkably, we show that two fundamentally distinct yet highly abundant processes - water evaporation and metabolic activity - can both regulate the autonomous division of GUVs. Our work may hint towards mechanisms that governed the division of protocells and adds to the strategic toolbox of bottom-up synthetic biology with its vision of bringing matter to life.

Explore related subjects

biophysicsPreprint

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Dreher, Y., Spatz, J. P., Göpfrich, K.. 2019-12-30. Protein-free division of giant unilamellar vesicles controlled by enzymatic activity. https://doi.org/10.1101/2019.12.30.881557

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

bioRxiv2026

Nanomechanical phenotyping uncovers a non-canonical smooth muscle-like hypercontractility program in lung squamous cell carcinoma myofibroblasts

Myofibroblast-like cancer-associated fibroblasts (myCAFs) drive the stiff, tumor-promoting microenvironment, yet their mechanical phenotype in non-small cell lung cancer (NSCLC) remains undefined. myCAFs from major NSCLC subtypes (lung adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC)) were examined combining atomic force microscopy and traction force microscopy with molecular and signaling analyses. LUAD-myCAFs displayed canonical myofibroblast features, including elevated stiffness, traction forces, ROCK-MYPT1 signaling, and -SMA-rich stress fibers. Unexpectedly, LUSC-myCAFs amplified these nanomechanical features despite reduced ROCK-MYPT1 signaling and comparable -SMA levels. Instead, they exhibited a smooth muscle cell (SMC)-like contractile program characterized by enhanced SM-MHC(MYH11) expression colocalized with -SMA, ERK1/2-RLC hyperactivation, and DNA methylation reprogramming including SMC-contractility regulators. LUSC-myCAF hypercontractility was linked with reduced proliferative capacity and smaller intratumoral vessel lumens, consistent with the low CAF density and enhanced hypoxia patterns reported in LUSC. SMC markers were enriched and associated with adverse outcomes selectively in LUSC, highlighting the relevance of SMC-like myCAFs in LUSC progression. These findings unveil subtype-specific myCAF programs in NSCLC, and identify -SMA/SM-MHC(MYH11) myCAFs as key determinants of tumor mechanics, providing a rationale for the survival benefits of antihypertensive drugs targeting SMC hypercontractility. Moreover, they demonstrate that nanomechanical phenotyping can uncover translationally relevant myCAF phenotypes invisible to molecular profiling.

biophysics↗
bioRxiv2026

Frequency-Dependent Structural Responses of Amyloid-β Fibrils to Terahertz Pulses: A Nonequilibrium Molecular Dynamics Study

The abnormal aggregation of amyloid proteins into fibrils is closely associated with several neurodegenerative diseases, highlighting the importance of developing effective strategies to modulate fibril structural stability. Here, we employed nonequilibrium molecular dynamics(NEMD) simulations to examine the effects of intense terahertz-to-mid-infrared pulses on three amyloid fibrils (2LMP, 2MXU, and 5OQV), focusing on the combined effects of pulse frequency and electric-field strength. Frequency scans from 0.5 to 60 THz in 0.5 THz steps revealed frequency-dependent losses of {beta}-sheet content, with several common response patterns in these fibrils. Comparisons at 2, 23, 33, and 50 THz showed that pulse-induced changes in secondary structure differed from those in high-temperature controls. Hydrogen-bond analysis showed that total hydrogen-bond counts could partially recover even as interchain hydrogen bonds continued to decrease, with distinct responses among representative chain pairs. We therefore propose a two-threshold electric-field framework for fibril disruption: Eth1 describes the onset of structural perturbation, whereas Eth2 indicates persistent structural loss after the pulse. This framework offers a testable approach for characterizing amyloid structural responses to external fields, although the underlying energy-coupling mechanisms, quantitative thresholds, and long-term recovery require further validation. These findings may provide a theoretical basis for exploring external-field-based strategies to modulate protein aggregation.

biophysics↗
bioRxiv2026

Organised streaming of cerebrospinal fluid in the human third ventricle

Quasi-periodic pressure pulses associated with cardiac and respiratory activity generate reciprocating cerebrospinal fluid (CSF) motion in the human ventricles. Regular waves dominated by the cardiac cycle are overlaid with cycles of low-frequency respiratory waves, the latter to become stronger in forced breathing or even dominated by large successive flushes in NREM sleep. The present study investigates how such waves contribute to residual streaming within the human ventricles. Transient CFD simulations were performed in the third ventricle at varying parameters of frequency, stroke volume and wave-form asymmetry. Increasing the aqueduct peak Reynolds-number, either by small stroke volume and high frequency or large stroke volume at low frequency, transfers the flow from a reversible flow pattern to the formation of clear preferential pathways, alternating between the in- and outflow cycle. The resulting permanent streaming flux across the aqueduct relative to the mean oscillatory flow-rate, i.e. the dimensionless streaming ratio SR follows a rational saturation relation, SR [~] ReAq,peak/(C + ReAq,peak), demonstrating that increasing the peak aqueduct Reynolds number yields diminishing returns and bounds the relative contribution of residual inter-ventricular streaming. These findings demonstrate differences in hydrodynamic organisation in the third ventricle and highlight the importance of this organisation for intraventricular fluid exchange.

biophysics↗