Pith. sign in

REVIEW

Nonlinear contractile response of actomyosin active gels to control signals

Not yet reviewed by Pith; the record is open.

This paper has not been read by Pith yet. Machine review is queued; the pith claim, tier, and objections will appear here once it completes.

SPECIMEN: schema-true, not a live event

T0 review · schema-true

One-sentence machine reading of the paper's core claim.

pith:XXXXXXXX · record.json · timestamp

arxiv 2502.18672 v1 pith:7PD3C4HO submitted 2025-02-25 cond-mat.soft physics.bio-ph

classification cond-mat.softphysics.bio-ph
keywords actomyosindeltacontractilecontrolresponsesignalsactivenonlinear
verification ladder T0 review T1 audit T2 compute T3 formal
0 comments
abstract

Biological systems tightly regulate their physiological state using control signals. This includes the actomyosin cytoskeleton, a contractile active gel that consumes chemical free energy to drive many examples of cellular mechanical behavior. Upstream regulatory pathways activate or inhibit actomyosin activity. However, the contractile response of the actomyosin cytoskeleton to control signals remains poorly characterized. Here we employ reconstituted actomyosin active gels and subject them to step and pulsatile activation inputs. We find evidence for a nonlinear impulse response, which we quantify via a transfer function $\delta \varepsilon / \delta g$ that relates input free-energy pulses $\delta g$ to output strain pulses $\delta \varepsilon$. We find a scaling relation $\delta \varepsilon / \delta g \sim g^{-0.3}$. The negative sign of the exponent represents a decreased effectiveness of a contracting gel in converting energy to strain. We ascribe nonlinearity in our system to a density-dependent mechanism, which contrasts strain-stiffening nonlinear responses to external stresses. Contractile response to control signals is an essential step toward understanding how information from mechanical signaling processes flow through actomyosin networks in living, and likely also synthetic, cells.

Discussion (0). Continue with ORCID to comment.

Pith tools