📰 "A mechanical bifurcation constrains the evolution of cell sheet folding in the family Volvocaceae"
https://arxiv.org/abs/2603.15171 #Physics.Bio-Ph
#Morphogenesis #Cond-Mat.Soft
#Mechanical #Q-Bio.To
#Cell
A mechanical bifurcation constrains the evolution of cell sheet folding in the family Volvocaceae
The processes of morphogenesis that give rise to the shapes of organs and organisms during development are often driven by mechanical instabilities. Can such mechanical bifurcations also drive or constrain the evolution of these processes in the first place? We discover an instance of these constraints in the green algae of the family Volvocaceae. During their development, their bowl-shaped embryonic cell sheet turns itself inside out. This inversion is driven by a simple wave of cell wedging in the genus Pleodorina (16-128 cells) and more complex programmes of cell shape changes in Volvox (~400-50000 cells). However, no species with intermediate cell numbers (256 cells) have been described. Here, we relate this gap to a mechanical bifurcation: Focusing on the inversion of Pleodorina californica (64 cells), we develop a continuum model, in which the cell shape changes driving inversion appear as changes of the intrinsic curvature of an elastic surface. A mechanical bifurcation in this model predicts that inversion is only possible in a subset of its parameter space. Strikingly, parameters estimated for P. californica fall into this possible subset, but those that we extrapolate to 256 or more cells using allometric observations and a model of cell cleavage in Volvocaceae do not. Our work thus suggests that the more complex inversion strategies of Volvox are an evolutionary necessity to obviate this bifurcation and indicates more broadly how mechanical bifurcations can drive the evolution of morphogenesis.
📰 "Mechanical forces orchestrate the epigenetic landscape of oral mesenchymal stem/progenitor cell fate in dental and periodontal tissues"
https://doi.org/doi:10.3389/fcell.2026.1743397https://pubmed.ncbi.nlm.nih.gov/41836287/ #Mechanical #Forces #Cell
Frontiers | Mechanical forces orchestrate the epigenetic landscape of oral mesenchymal stem/progenitor cell fate in dental and periodontal tissues
The oral cavity serves as the primary source of oral mesenchymal stem/progenitor cell populations residing in the dental pulp, periodontal ligament, deciduou...
📰 "Theca cell mechanosensing and regulation of follicular extracellular matrix during ovarian follicle development"
https://www.biorxiv.org/content/10.64898/2026.03.12.711479v1?rss=1 #Mechanosensing #Extracellular #Mechanical #CellTheca cell mechanosensing and regulation of follicular extracellular matrix during ovarian follicle development
Mammalian folliculogenesis is essential for female hormonal regulation and successful reproduction. While the steroidogenic functions of theca cells (TCs) have been implicated in ovarian diseases and infertility, the physico-structural properties of TCs and their associated extracellular matrix (ECM), or theca matrix, remain poorly understood. Using murine ovaries, we show that a stiff basement membrane (BM) and theca matrix constitute a mechanically instructive niche that modulates TC proliferation and Yes-associated protein (YAP) signalling in secondary follicles. We identify hyaluronic acid (HA) as a key matrix component that is actively secreted by contractile TCs. The HA scaffold, in turn, regulates TC proliferation, YAP signalling and motility, and is required for overall follicle growth. We showed that stiffer substrates enhance YAP nuclear transport in TCs, while mechanical stretch, cell packing, and curvature affect TC proliferation. In addition, TCs exhibit directed migration towards regions of positive curvature. Together, this study reveals a mechanochemical feedback mechanism that establishes TC mechanics and HA as key regulators of theca matrix formation that is essential for mammalian folliculogenesis.
### Competing Interest Statement
The authors have declared no competing interest.
National Research Foundation, NRF-MSG-2023-0001
Ministry of Eduction, Singapore, T2EP30222-0026
📰 "An apical junction protein antagonizes mechanosensitive calcium signaling to establish stochastic choices of olfactory neuron subtypes"
https://www.biorxiv.org/content/10.64898/2026.03.12.710951v1?rss=1 #Mechanical #CellAn apical junction protein antagonizes mechanosensitive calcium signaling to establish stochastic choices of olfactory neuron subtypes
Mechanical forces regulate brain development and left-right body patterning. However, the role of mechanical signaling in brain lateralization remains unclear. In Caenorhabditis elegans , the left and right AWC olfactory neurons communicate via a gap junction network to stochastically differentiate into the default AWCOFF and induced AWCON subtypes. SLO BK potassium channels, SLO-1 and SLO-2, act redundantly to inhibit a calcium-regulated protein kinase pathway in the specification of the AWCON subtype. Here, we identified a role for AJM-1 (apical junction molecule 1) in promoting AWCON from an unbiased forward genetic screen for mutants that suppress the slo-1(gf) 2AWCON phenotype. AJM-1 is located at three distinct tight junctions between amphid neurons (including AWC) and sheath glia, sheath and socket glia, and socket glia and hypodermal cells (also known as epidermal cells) at the anterior tip of the animal. In addition to its cell-autonomous function, the non-cell-autonomous function of AJM-1 in glial and hypodermal cells is required for the specification of the AWCON subtype. Furthermore, we identified a role for the DEL-1 mechanosensitive DEG/ENaC channel in the calcium signaling pathway, mediated by UNC-2 and EGL-19 voltage-activated calcium channels, that specifies AWCOFF. Together, our results suggest a mechanism in which AJM-1 promotes SLO-1 expression and antagonizes mechanosensitive calcium signaling, thereby promoting the AWCON subtype. This study provides insight into the role of mechanical force in the stochastic lateralization of olfactory neurons.
### Competing Interest Statement
The authors have declared no competing interest.
📰 "An all-in-one injectable biocement: self-setting magnesium phosphate for bone repair, fracture adhesion and osteoporotic fixation"
https://doi.org/doi:10.1093/rb/rbaf133https://pubmed.ncbi.nlm.nih.gov/41835087/ #Mechanical #Adhesion📰 "Programmable Coacervate-Membrane Interactions Direct Internal and Collective Organization in Membranized Protocells"
https://doi.org/doi:10.1002/anie.202525899https://pubmed.ncbi.nlm.nih.gov/41834455/ #Cytoskeletal #Mechanical📰 "Vimentin Intermediate Filaments: A Paradigm Shift From Static Structure to Dynamic Cytoplasmic Network"
https://doi.org/doi:10.1002/bies.70125https://pubmed.ncbi.nlm.nih.gov/41834240/ #Mechanical #Vimentin #Cell📰 "Synthetic aptamer mechanoreceptors enable cell-specific force sensing and temporal control via DNA circuits"
https://doi.org/doi:10.1038/s41467-026-70765-whttps://pubmed.ncbi.nlm.nih.gov/41833970/ #Mechanical #Force #Cell📰 "Mechanical Signaling Drives Tunneling Nanotubes to Preserve Cytoskeleton Tension and Lamin Integrity Against α-Synuclein-Induced Senescence in Astroglia"
https://www.biorxiv.org/content/10.64898/2026.03.13.711517v1?rss=1 #Cytoskeleton #Mechanical #LaminMechanical Signaling Drives Tunneling Nanotubes to Preserve Cytoskeleton Tension and Lamin Integrity Against α-Synuclein-Induced Senescence in Astroglia
Astroglia can counteract the harmful effects of α-synuclein (α-SYN) protofibrils and reverse premature cellular senescence by promoting tunneling nanotubes (TNTs). However, the mechanism behind this recovery is unknown. This study is the first to examine TNT-mediated mechanical stability in senescent astroglial recovery. We demonstrate that disruption of Lamin A/C in α-SYN-protofibrils-treated senescent cells reduces actin-cytoskeleton stress, as measured by nucleus flatness index and isometric scale factor from quantitative microscopy. ROCK (Rho-associated kinase) inhibition, which is crucial for reducing actin-cytoskeleton tension, promotes TNTs. Small molecules like Cytochalasin-D, Nocodazole, and Jasplakinolide, which inhibit TNTs by altering actin tension other than ROCK pathway, cannot reverse senescence. RNA-sequence heatmaps reveal changes in senescence-, integrin-, and ROCK-pathway genes; STRING links these to the Hippo pathway. Experimental results show that cytosolic YAP translocation, a key regulator of Hippo pathway, is vital for TNT formation and actin-based stability in U87-MG astrocytoma and primary astrocytes. Interestingly, TNTs form between two cells with different actin tensions: one exhibits low actin tension with Hippo signaling on, while the other has higher actin tension with Hippo signaling off. The most notable observation is the high abundance of YAP inside the TNTs, along with actin. The study shows that TNTs maintain mechanical stability through Lamin A/C integrity and actin tension in α-SYN-induced senescent astroglia, thereby protecting the cells, reversing senescence.
### Competing Interest Statement
The authors have declared no competing interest.
Indian Council of Medical Research, https://ror.org/0492wrx28, IIRP-2023-0084
Rxiv mechanobio