Understanding the Role of Polyamine N-Acetyltransferase in the Fission Yeast Response to Perturbation of the Cytokinetic Machinery
Abstract
The mechanisms that ensure cytokinetic fidelity are important for cellular proliferation and the maintenance of genomic integrity. To better understand these mechanisms, the actin depolymerizing drug, LatA, was previously used to screen for fission yeast genes required to prevent cytokinesis failure. This screen identified the pna1 polyamine-N-acetyltransferase. Here, I show that pna1Δ mutants display severe growth defects when exposed to even low doses of LatA. Furthermore, LatA-treated pna1Δ cells display increased rates of cytokinesis failure characterized by fragmentation of the cytokinetic actomyosin ring. Surprisingly, Pna1-GFP fusion proteins form cytoplasmic filaments that may represent cytoophidia (meaning "cellular snakes"), a class of structures implicated in metabolic regulation via compartmentalization. Interestingly, Pna1p filament length is dependent on growth phase, but is not affected by inhibition of the TOR pathway. I suggest that fission yeast respond to LatA-induced cytoskeletal perturbations through modulating polyamine interaction with actin via a mechanism involving Pna1p-mediated polyamine acetylation.