Pathogenic Yersinia species employ several strategies to evade the host immune system, including interfering with cytoskeletal remodeling as a way to block macrophage phagocytosis. The kinase YopO binds directly to monomeric actin and phosphorylates the actin-remodeling protein gelsolin, but the functional importance of this gelsolin modification has not been clear. A combined biochemical, computational, and biophysical study now reveals that YopO-mediated phosphorylation activates host gelsolin, leading to severed actin filaments and disturbed actin dynamics.
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