Golgi inheritance in mammalian cells is mediated through endoplasmic reticulum export activities

Nihal Altan-Bonnet, Rachid Sougrat, Wei Liu, Erik L. Snapp, Theresa Ward, Jennifer Lippincott-Schwartz

Research output: Contribution to journalArticle

91 Scopus citations

Abstract

Golgi inheritance during mammalian cell division occurs through the disassembly, partitioning, and reassembly of Golgi membranes. The mechanisms responsible for these processes are poorly understood. To address these mechanisms, we have examined the identity and dynamics of Golgi proteins within mitotic membranes using live cell imaging and electron microscopy techniques. Mitotic Golgi fragments, seen in prometaphase and telophase, were found to localize adjacent to endoplasmic reticulum (ER) export domains, and resident Golgi transmembrane proteins cycled rapidly into and out of these fragments. Golgi proteins within mitotic Golgi haze-seen during metaphase-were found to redistribute with ER markers into fragments when the ER was fragmented by ionomycin treatment. The temperature-sensitive misfolding mutant ts045VSVG protein, when localized to the Golgi at the start of mitosis, became trapped in the ER at the end of mitosis in cells shifted to 40°C. Finally, reporters for Arf1 and Sar1 activity revealed that Arf1 and Sar1 undergo sequential inactivation during mitotic Golgi breakdown and sequential reactivation upon Golgi reassembly at the end of mitosis. Together, these findings support a model of mitotic Golgi inheritance that involves inhibition and subsequent reactivation of cellular activities controlling the cycling of Golgi components into and out of the ER.

Original languageEnglish (US)
Pages (from-to)990-1005
Number of pages16
JournalMolecular biology of the cell
Volume17
Issue number2
DOIs
StatePublished - Feb 2006

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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    Altan-Bonnet, N., Sougrat, R., Liu, W., Snapp, E. L., Ward, T., & Lippincott-Schwartz, J. (2006). Golgi inheritance in mammalian cells is mediated through endoplasmic reticulum export activities. Molecular biology of the cell, 17(2), 990-1005. https://doi.org/10.1091/mbc.E05-02-0155