Proteasome assembly chaperone translation upon stress requires Ede1 phase separation at the plasma membrane.

Proteome adaptation is key to cells surviving stresses. Increased translation of proteasome assembly chaperones (PACs) is critical for increasing proteasome assembly and cell degradative capacity. The endocytic protein Ede1 recruits PAC mRNA to cortical actin patches in Saccharomyces cerevisiae for translation upon stress. We show, through genetic and pharmacological studies, that this is mediated by the capacity of Ede1 to phase separate. PAC expression is maintained when we exchange the phase separating domains from Ede1 for those of unrelated proteins. Without these phase separating regions, PAC expression is not induced upon stress, preventing increased proteasome assembly, causing cell death. This work identifies a mechanism underpinning Ede1-mediated increased translation of specific mRNAs at a time when general translation is repressed.

Mechanosignals in abdominal aortic aneurysms.

Cumulative evidence has shown that mechanical and frictional forces exert distinct effects in the multi-cellular aortic layers and play a significant role in the development of abdominal aortic aneurysms (AAA). These mechanical cues collectively trigger signaling cascades relying on mechanosensory cellular hubs that regulate vascular remodeling programs leading to the exaggerated degradation of the extracellular matrix (ECM), culminating in lethal aortic rupture. In this review, we provide an update and summarize the current understanding of the mechanotransduction networks in different cell types during AAA development. We focus on different mechanosensors and stressors that accumulate in the AAA sac and the mechanotransduction cascades that contribute to inflammation, oxidative stress, remodeling, and ECM degradation. We provide perspectives on manipulating this mechano-machinery as a new direction for future research in AAA.