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Published online 11 February 2002. doi:10.1083/jcb.200112028
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© The Rockefeller University Press, 0021-9525/2002/2/643 $5.00
The Journal of Cell Biology, Volume 156, Number 4, February 18, 2002 643-651

Article

 PEX11 promotes peroxisome division independently of peroxisome metabolism

Xiaoling Li and Stephen J. Gould

Department of Biological Chemistry, The Johns Hopkins University School of Medicine, Baltimore, MD 21205

Address correspondence to Stephen J. Gould, Dept. of Biological Chemistry, The Johns Hopkins University School of Medicine, 725 North Wolfe St., Baltimore, MD 21205. Tel.: (410) 955–3424. Fax: (410) 955–0215. E-mail: sgould{at}jhmi.edu

The PEX11 peroxisomal membrane proteins are the only factors known to promote peroxisome division in multiple species. It has been proposed that PEX11 proteins have a direct role in peroxisomal fatty acid oxidation, and that they only affect peroxisome abundance indirectly. Here we show that PEX11 proteins are unique in their ability to promote peroxisome division, and that PEX11 overexpression promotes peroxisome division in the absence of peroxisomal metabolic activity. We also observed that mouse cells lacking PEX11ß display reduced peroxisome abundance, even in the absence of peroxisomal metabolic substrates, and that PEX11ß-/- mice are partially deficient in two distinct peroxisomal metabolic pathways, ether lipid synthesis and very long chain fatty acid oxidation. Based on these and other observations, we propose that PEX11 proteins act directly in peroxisome division, and that their loss has indirect effects on peroxisome metabolism.

Key Words: peroxisome biogenesis; fatty acid oxidation; organelle division; peroxisomal membrane protein; Zellweger syndrome


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