Age-Onset Phosphorylation of a Minor Actin Variant Promotes Intestinal Barrier Dysfunction.

ABSTRACT: Age-associated decay of intercellular interactions impairs the cells' capacity to tightly associate within tissues and form a functional barrier. This barrier dysfunction compromises organ physiology and contributes to systemic failure. The actin cytoskeleton represents a key determinant in maintaining tissue architecture. Yet, it is unclear how age disrupts the actin cytoskeleton and how this, in turn, promotes mortality. Here, we show that an uncharacterized phosphorylation of a low-abundant actin variant, ACT-5, compromises integrity of the C. elegans intestinal barrier and accelerates pathogenesis. Age-related loss of the heat-shock transcription factor, HSF-1, disrupts the JUN kinase and protein phosphatase I equilibrium which increases ACT-5 phosphorylation within its troponin bindin

SUBMITTER: Egge N 

PROVIDER: S-EPMC6897307 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature