Evidence for prebudding arrest of ER export in animal cell mitosis and itsrole in generating golgi partitioning intermediates

Citation
Ar. Prescott et al., Evidence for prebudding arrest of ER export in animal cell mitosis and itsrole in generating golgi partitioning intermediates, TRAFFIC, 2(5), 2001, pp. 321-335
Citations number
50
Categorie Soggetti
Cell & Developmental Biology
Journal title
TRAFFIC
ISSN journal
13989219 → ACNP
Volume
2
Issue
5
Year of publication
2001
Pages
321 - 335
Database
ISI
SICI code
1398-9219(200105)2:5<321:EFPAOE>2.0.ZU;2-X
Abstract
During mitosis the interconnected Golgi complex of animal cells breaks down to produce both finely dispersed elements and discrete vesiculotubular str uctures. The endoplasmic reticulum (ER) plays a controversial role in gener ating these partitioning intermediates and here we highlight the importance of mitotic ER export arrest in this process. We show that experimental inh ibition of ER export (by microinjecting dominant negative Sar1 mutant prote ins) is sufficient to induce and maintain transformation of Golgi cisternae to vesiculotubular remnants during interphase and telophase, respectively. We also show that buds on the ER, ER exit sites and COPII vesicles are mar kedly depleted in mitotic cells and COPII components Sec23p, Sec24p, Sec13p and Sec31p redistribute into the cytosol, indicating ER export is inhibite d at an early stage. Finally, we find a markedly uneven distribution of Gol gi residents over residual exit sites of metaphase cells, consistent with t ubulovesicular Golgi remnants arising by fragmentation rather than redistri bution via the ER. Together, these results suggest selective recycling of G olgi residents, combined with prebudding cessation of ER export, induces tr ansformation of Golgi cisternae to vesiculotubular remnants in mitotic cell s. The vesiculotubular Golgi remnants, containing populations of slow or no nrecycling Golgi components, arise by fragmentation of a depleted Golgi rib bon independently from the ER.