We investigate collective dynamics of branched actin networks growing against a rigid movable wall constrained by a resistive force. Computing the force velocity relations, we show that the stall force of such networks depends not only on the average number of filaments touching the wall, but also on the amount of fluctuation of the leading edge of the network. These differences arise due to differences in the network architecture, namely, distance between two adjacent branching points and the initial distance of the starting filament from the wall, with their relative magnitudes influencing the nature of the force velocity curves (convex versus concave). We also show that the introduction of branching results in nonmonotonic diffusion constant, a quantity that measures the growth in length fluctuation of the leading edge of the network, as a function of externally applied force. Together our results demonstrate how the collective dynamics of a branched network differs from that of a parallel filament network.
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http://dx.doi.org/10.1103/PhysRevE.90.062718 | DOI Listing |
J Cell Biol
April 2025
Department of Genetics and Cell Biology, College of Life Sciences, State Key Laboratory of Medicinal Chemical Biology, Nankai University, Tianjin, China.
TBC1D20 deficiency causes Warburg Micro Syndrome in humans, characterized by multiple eye abnormalities, severe intellectual disability, and abnormal sexual development, but the molecular mechanisms remain unknown. Here, we identify TBC1D20 as a novel Rab11 GTPase-activating protein that coordinates vesicle transport and actin remodeling to regulate ciliogenesis. Depletion of TBC1D20 promotes Rab11 vesicle accumulation and actin deconstruction around the centrosome, facilitating the initiation of ciliogenesis even in cycling cells.
View Article and Find Full Text PDFJ Cell Sci
January 2025
Department of Cellular & Physiological Sciences, Life Sciences Institute, University of British Columbia, Vancouver, BC V6T 1Z3, Canada.
Here, we apply SuperResNET network analysis of dSTORM single-molecule localization microscopy (SMLM) to determine how the clathrin endocytosis inhibitors pitstop 2, dynasore and Latrunculin A alter the morphology of clathrin-coated pits. SuperResNET analysis of HeLa and Cos7 cells identifies: small oligomers (Class I); pits and vesicles (Class II); and larger clusters corresponding to fused pits or clathrin plaques (Class III). Pitstop 2 and dynasore induce distinct homogeneous populations of Class II structures in HeLa cells suggesting that they arrest endocytosis at different stages.
View Article and Find Full Text PDFPediatr Nephrol
January 2025
Department of Pediatrics, University of Cologne, Faculty of Medicine and University Hospital Cologne, Kerpener Street 62, 50937, Cologne, Germany.
The integrity of the filtration barrier of the kidney relies on the proper composition of podocyte interdigitating foot processes. Their architecture is supported by a complex actin-cytoskeleton. Following podocyte stress or injury, podocytes encounter structural changes, including rearrangement of the actin network and subsequent effacement of the foot processes.
View Article and Find Full Text PDFCells
January 2025
Cellular and Molecular Biotechnology Research Institute, National Institute of Advanced Industrial Science and Technology (AIST), Central 5 1-1-1 Higashi, Tsukuba 305-8565, Ibaraki, Japan.
Nestin is a type VI intermediate filament protein and a well-known neural stem cell marker. It is also expressed in high-grade cancer cells, forming copolymerized filaments with vimentin. We previously showed that nestin inhibits the binding of vimentin's tail domain to actin filaments (AFs) by steric hindrance through its large nestin tail domain (NTD), thereby increasing three-dimensional cytoskeleton network mobility, enhancing cell flexibility, and promoting cancer progression.
View Article and Find Full Text PDFResearch (Wash D C)
January 2025
Department of Ophthalmology, The Future Medicine Laboratory, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, People's Republic of China.
Excessive fibrosis is the primary factor for the failure of glaucoma drainage device (GDD) implantation. Thus, strategies to suppress scar formation in GDD implantation are crucial. Although it is known that in implanted medical devices, microscale modification of the implant surface can modulate cell behavior and reduce the incidence of fibrosis, in the field of ophthalmic implants, especially the modification and effects of hydrogel micropatterns have rarely been reported.
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