Salomon, A. K. | Search bioRxiv

bioRxiv2018

Microtubules provide a viscoelastic resistance to myocyte motion.

BackgroundMicrotubules (MT) buckle and bear load during myocyte contraction, a behavior enhanced by post-translational detyrosination. This buckling suggests a spring-like resistance against myocyte shortening, which could store energy and aid myocyte relaxation. Despite this visual suggesting of elastic behavior, the precise mechanical contribution of the cardiac MT network remains to be defined.\n\nMethodsHere we experimentally and computationally probe the mechanical contribution of stable microtubules and their influence on myocyte function. We use multiple approaches to interrogate viscoelasticity and cell shortening in primary murine myocytes where either MTs are depolymerized or detyrosination is suppressed, and use the results to inform a mathematical model of myocyte viscoelasticity.\n\nResultsMT ablation by colchicine concurrently enhances both the degree of shortening and speed of relaxation, a finding inconsistent with simple spring-like microtubule behavior, and suggestive of a viscoelastic mechanism. Axial stretch and transverse indentation confirm that microtubules increase myocyte viscoelasticity. Specifically, increasing the rate of strain amplifies the MT contribution to myocyte stiffness. Suppressing MT detyrosination with parthenolide or via overexpression of tubulin tyrosine ligase (TTL) has mechanical consequences that closely resemble colchicine, suggesting that the mechanical impact of MTs relies on a detyrosination-dependent linkage with the myocyte cytoskeleton. Mathematical modeling affirms that alterations in cell shortening conferred by either MT destabilization or tyrosination can be attributed to internal changes in myocyte viscoelasticity.\n\nConclusionsThe results suggest that the cardiac MT network regulates contractile amplitudes and kinetics by acting as a cytoskeletal shock-absorber, whereby MTs provide breakable cross-links between the sarcomeric and non-sarcomeric cytoskeleton that resist rapid length changes during both shortening and stretch.

biophysics↗

bioRxiv2018

Spatial variation in exploited metapopulations obscures risk of collapse

Unanticipated declines among exploited species have commonly occurred despite harvests that appeared sustainable prior to collapse. This is particularly true in the oceans where spatial scales of management are often mismatched with spatially complex metapopulations. We explore causes, consequences and potential solutions for spatial mismatches in harvested metapopulations in three ways. First, we generate novel theory illustrating when and how harvesting metapopulations increases spatial variability and in turn masks local scale volatility. Second, we illustrate why spatial variability in harvested metapopulations leads to negative consequences using an empirical example of a Pacific herring metapopulation. Finally, we construct a numerical management strategy evaluation model to identify and highlight potential solutions for mismatches in spatial scale and spatial variability. Our results highlight that spatial complexity can promote stability at large scales, however ignoring spatial complexity produces cryptic and negative consequences for people and animals that interact with resources at small scales. Harvesting metapopulations magnifies spatial variability, which creates discrepancies between regional and local trends while increasing risk of local population collapses. Such effects asymmetrically impact locally constrained fishers and predators, which are more exposed to risks of localized collapses. Importantly, we show that dynamically optimizing harvest can minimize local risk without sacrificing yield. Thus, multiple nested scales of management may be necessary to avoid cryptic collapses in metapopulations and the ensuing ecological, social and economic consequences.

ecology↗