期刊
JOURNAL OF CELL BIOLOGY
卷 190, 期 3, 页码 363-375出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200911024
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资金
- National Cancer Institute's Initiative for Chemical Genetics [N01-CO-12400]
- National Institutes of Health (NIH) [GM08759, GM083254, GM083977]
- University of Colorado at Boulder
- National Center for Research Resources [P41-RR000592]
The endoplasmic reticulum (ER) network is extremely dynamic in animal cells, yet little is known about the mechanism and function of its movements. The most common ER dynamic, termed ER sliding, involves ER tubule extension along stable microtubules (MTs). In this study, we show that ER sliding occurs on nocodazole-resistant MTs that are posttranslationally modified by acetylation. We demonstrate that high MT curvature is a good indicator of MT acetylation and show in live cells that ER sliding occurs predominantly on these curved, acetylated MTs. Furthermore, increasing MT acetylation by drug treatment increases the frequency of ER sliding. One purpose of the ER sliding on modified MT tracts could be to regulate its interorganelle contacts. We find that all mitochondria and many endosomes maintain contact with the ER despite the movements of each. However, mitochondria, but not endosomes, preferentially localize to acetylated MTs. Thus, different ER dynamics may occur on distinct MT populations to establish or maintain contacts with different organelles.
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