The origin and maintenance of mammalian peroxisomes involves a de novo PEX16-dependent pathway from the ER

被引:243
作者
Kim, Peter K.
Mullen, Robert T.
Schumann, Uwe
Lippincott-Schwartz, Jennifer [1 ]
机构
[1] NICHHD, Cell Biol & Metab Branch, NIH, Bethesda, MD 20892 USA
[2] Univ Guelph, Dept Cellular & Mol Biol, Guelph, ON N1G 2W1, Canada
关键词
D O I
10.1083/jcb.200601036
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Peroxisomes are ubiquitous organelles that proliferate under different physiological conditions and can form de novo in cells that lack them. The endoplasmic reticulum ( ER) has been shown to be the source of peroxisomes in yeast and plant cells. It remains unclear, however, whether the ER has a similar role in mammalian cells and whether peroxisome division or outgrowth from the ER maintains peroxisomes in growing cells. We use a new in cellula pulse-chase imaging protocol with photoactivatable GFP to investigate the mechanism underlying the biogenesis of mammalian peroxisomes. We provide direct evidence that peroxisomes can arise de novo from the ER in both normal and peroxisome-less mutant cells. We further show that PEX16 regulates this process by being cotranslationally inserted into the ER and serving to recruit other peroxisomal membrane proteins to membranes. Finally, we demonstrate that the increase in peroxisome number in growing wild-type cells results primarily from new peroxisomes derived from the ER rather than by division of preexisting peroxisomes.
引用
收藏
页码:521 / 532
页数:12
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