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Updated: Mar 11, 2026

Methods to Classify Cytoplasmic Foci as Mammalian Stress Granules
Published on: May 12, 2017
Arp2/3 complex and Mps3 are required for regulation of ribosome biosynthesis in the secretory stress response
Yukari Yabuki1, Masako Katayama1, Yushi Kodama1
1Department of Biofunctional Science and Technology, Graduate School of Biosphere Science, Hiroshima University, Kagamiyama 1-4-4, Higashi-Hiroshima, 739-8528, Japan.
Abstract:
Secretory defects cause transcriptional repression of ribosome biogenesis in Saccharomyces cerevisiae. However, the molecular mechanism underlying secretory defect-induced transcriptional repression of ribosome biogenesis remains to be fully elucidated. In this study, we demonstrated that the Arp2/3 complex was required for reduction of ribosome protein gene expression in response to defective secretion by addition of tunicamycin. Two cmd1 mutants, cmd1-228 and cmd1-239 that cause mislocalization of calmodulin and defective mitotic spindle formation, respectively, failed to interact with Arc35, a component of the Arp2/3 complex. These mutants also caused defects in the reduction of ribosome protein gene expression induced by secretory blockade. A mutation in TUB4 (tub4-1), whose product has an essential function in microtubule organization, showed a similar response. In addition, we showed that the response to a secretory defect required SUN protein Mps3, which was localized at the nuclear envelope and involved in spindle pole body assembly. These results suggest that the Arp2/3 complex is required to transmit signals resulting from secretory blockade, and that the spindle pole body functions as a transit point from cytoplasm to Mps3 at the nuclear envelope. Copyright © 2016 John Wiley & Sons, Ltd.
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