Acute heat shock leads to cortical domain internalization and polarity loss in the C. elegans embryo

Abstract

Summary: Many developmental processes are inherently robust due to network organization of the participating factors and functional redundancy. The heterogeneity of the factors involved and their connectivity puts these processes at risk of abrupt system collapse under stress. The polarization of the one-cell C. elegans embryo constitutes such an inherently robust process with functional redundancy. However, how polarization is affected by acute stress has not been thoroughly investigated. Here, we report that heat shock (348C, 1 h) triggers a highly reproducible loss of the anterior and collapse of the posterior polarity domains. Temperature-dependent loss of cortical nonmuscle myosin II drastically reduces cortical tension and leads to internalization of large plasma membrane domains including the membrane-associated polarity factor PAR-2. After internalization, plasma membrane vesicles and associated factors cluster around centrosomes and are thereby withdrawn from the polarization process. Transient formation of the posterior polarity domain suggests that microtubule-induced self-organization of this domain is not compromised after heat shock. Hence, our data uncover that the polarization system undergoes a temperature-dependent collapse under acute stress. genesis 54:220-228, 2016. V C 2016Wiley Periodicals, Inc.

Heat shock‐induced mitotic arrest requires heat shock protein 105 for the activation of spindle assembly checkpoint

“…Because heat shock blocks tubulin polymerization in a temperature-dependent manner (49), the mild heat shock used here may preferentially disrupt astral microtubules, and thus cause spindle misorientation. Heat shock disrupts the cortex function and delays first cell division in the Caenorhabditis elegans embryo (50). Moreover, the regulator of cortical dynein/dynactin localization dynamitin/p50 (51) is lost as a result of mild heat shock (14).…”

Uniaxial loading induces a scalable switch in cortical actomyosin flow polarization and reveals mechanosensitive regulation of cytokinesis

“…The division of the one-cell C. elegans embryo represents a highly suitable model to quantitatively dissect spatiotemporal dynamics of the cytokinetic actomyosin cortex and to uncover underlying regulatory principles [9, 18, 27–33]. Previously, it has been shown through highly informative ablation experiments of the contractile ring that it is able to repair requiring an increased tension in the ring and reduced cortical tension in the vicinity [34].…”