19 research outputs found
Dynamic buckling of actin within filopodia
Filopodia are active tubular structuresprotruding from the cell surface which allow the cell to sense and interact with the surrounding environment through repetitive elongation-retraction cycles. The mechanical behavior of filo-podia has been studied by measuring the traction forces exerted on external sub-strates.1 These studies have revealed that internal actin flow can transduce a force across the cell surface through transmem-brane linkers like integrins. In addition to the elongation-retraction behavior filo-podia also exhibit a buckling and rota-tional behavior. Filopodial buckling in conjunction with rotation enables th
Quantitative Analysis of Cellular Traction Generation and Actomyosin Dynamics in a 3D Fibrin Matrix
Differential elasticity in lineage segregation of embryonic stem cells
The question of what guides lineage segregation is central to development,
where cellular differentiation leads to segregated cell populations destined
for specialized functions. Here, using optical tweezers measurements of mouse
embryonic stem cells (mESCs), we reveal a mechanical mechanism based on
differential elasticity in the second lineage segregation of the embryonic
inner cell mass into epiblast (EPI) cells - that will develop into the fetus -
and primitive endoderm (PrE) - which will form extraembryonic structures such
as the yolk sac. Remarkably, we find that these mechanical differences already
occur during priming and not just after a cell has committed to
differentiation. Specifically, we show that the mESCs are highly elastic
compared to any other reported cell type and that the PrE cells are
significantly more elastic than EPI-primed cells. Using a model of two cell
types differing only in elasticity we show that differential elasticity alone
can lead to segregation between cell types, suggesting that the mechanical
attributes of the cells contribute to the segregation process. Our findings
present differential elasticity as a previously unknown mechanical contributor
to the lineage segregation during the embryo morphogenesis
Dynamics of cancerous tissue correlates with invasiveness
Two of the classical hallmarks of cancer are uncontrolled cell division and tissue invasion, which turn the disease into a systemic, life-threatening condition. Although both processes are studied, a clear correlation between cell division and motility of cancer cells has not been described previously. Here, we experimentally characterize the dynamics of invasive and non-invasive breast cancer tissues using human and murine model systems. The intrinsic tissue velocities, as well as the divergence and vorticity around a dividing cell correlate strongly with the invasive potential of the tissue, thus showing a distinct correlation between tissue dynamics and aggressiveness. We formulate a model which treats the tissue as a visco-elastic continuum. This model provides a valid reproduction of the cancerous tissue dynamics, thus, biological signaling is not needed to explain the observed tissue dynamics. The model returns the characteristic force exerted by an invading cell and reveals a strong correlation between force and invasiveness of breast cancer cells, thus pinpointing the importance of mechanics for cancer invasion
Helical buckling of actin inside filopodia generates traction
Cells can interact with their surroundings via filopodia, which are membrane protrusions that extend beyond the cell body. Filopodia are essential during dynamic cellular processes like motility, invasion, and cell鈥揷ell communication. Filopodia contain cross-linked actin filaments, attached to the surrounding cell membrane via protein linkers such as integrins. These actin filaments are thought to play a pivotal role in force transduction, bending, and rotation. We investigated whether, and how, actin within filopodia is responsible for filopodia dynamics by conducting simultaneous force spectroscopy and confocal imaging of F-actin in membrane protrusions. The actin shaft was observed to periodically undergo helical coiling and rotational motion, which occurred simultaneously with retrograde movement of actin inside the filopodium. The cells were found to retract beads attached to the filopodial tip, and retraction was found to correlate with rotation and coiling of the actin shaft. These results suggest a previously unidentified mechanism by which a cell can use rotation of the filopodial actin shaft to induce coiling and hence axial shortening of the filopodial actin bundle