Hurricane-induced power outage risk under climate change is primarily driven by the uncertainty in projections of future hurricane frequency.

Nine in ten major outages in the US have been caused by hurricanes. Long-term outage risk is a function of climate change-triggered shifts in hurricane frequency and intensity; yet projections of both remain highly uncertain. However, outage risk models do not account for the epistemic uncertainties in physics-based hurricane projections under climate change, largely due to the extreme computational complexity. Instead they use simple probabilistic assumptions to model such uncertainties. Here, we propose a transparent and efficient framework to, for the first time, bridge the physics-based hurricane projections and intricate outage risk models. We find that uncertainty in projections of the frequency of weaker storms explains over 95% of the uncertainty in outage projections; thus, reducing this uncertainty will greatly improve outage risk management. We also show that the expected annual fraction of affected customers exhibits large variances, warranting the adoption of robust resilience investment strategies and climate-informed regulatory frameworks.

Author Correction: Nuclear lamin A/C harnesses the perinuclear apical actin cables to protect nuclear morphology.

In the original version of this Article, the affiliation details for Arghavan Louhghalam were incorrectly given as 'Institute for NanoBioTechnology, The Johns Hopkins University, Baltimore, MD, 21218, USA', and it should have been given as 'Department of Civil and Environmental Engineering, University of Massachusetts Dartmouth, Dartmouth, MA 02747, USA'. Furthermore, an incorrect grant number, R1610512, was acknowledged. The correct grant number is NRF-2016R1C1B2015018. These errors have now been corrected in both the PDF and HTML versions of the Article.

Nuclear lamin A/C harnesses the perinuclear apical actin cables to protect nuclear morphology.

The distinct spatial architecture of the apical actin cables (or actin cap) facilitates rapid biophysical signaling between extracellular mechanical stimuli and intracellular responses, including nuclear shaping, cytoskeletal remodeling, and the mechanotransduction of external forces into biochemical signals. These functions are abrogated in lamin A/C-deficient mouse embryonic fibroblasts that recapitulate the defective nuclear organization of laminopathies, featuring disruption of the actin cap. However, how nuclear lamin A/C mediates the ability of the actin cap to regulate nuclear morphology remains unclear. Here, we show that lamin A/C expressing cells can form an actin cap to resist nuclear deformation in response to physiological mechanical stresses. This study reveals how the nuclear lamin A/C-mediated formation of the perinuclear apical actin cables protects the nuclear structural integrity from extracellular physical disturbances. Our findings highlight the role of the physical interactions between the cytoskeletal network and the nucleus in cellular mechanical homeostasis.