Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2016 May;1863(5):984-91.
doi: 10.1016/j.bbamcr.2015.09.032. Epub 2015 Oct 3.

Peroxisome homeostasis: Mechanisms of division and selective degradation of peroxisomes in mammals

Affiliations
Free article
Review

Peroxisome homeostasis: Mechanisms of division and selective degradation of peroxisomes in mammals

Masanori Honsho et al. Biochim Biophys Acta. 2016 May.
Free article

Abstract

Peroxisome number and quality are maintained by its biogenesis and turnover and are important for the homeostasis of peroxisomes. Peroxisomes are increased in number by division with dynamic morphological changes including elongation, constriction, and fission. In the course of peroxisomal division, peroxisomal morphogenesis is orchestrated by Pex11β, dynamin-like protein 1 (DLP1), and mitochondrial fission factor (Mff). Conversely, peroxisome number is reduced by its degradation. Peroxisomes are mainly degraded by pexophagy, a type of autophagy specific for peroxisomes. Upon pexophagy, an adaptor protein translocates on peroxisomal membrane and connects peroxisomes to autophagic machineries. Molecular mechanisms of pexophagy are well studied in yeast systems where several specific adaptor proteins are identified. Pexophagy in mammals also proceeds in a manner dependent on adaptor proteins. In this review, we address the recent progress in studies on peroxisome morphogenesis and pexophagy.

Keywords: Adaptor protein; Growth and division; Peroxisomal division; Peroxisomal morphogenesis; Peroxisome turnover; Pexophagy.

PubMed Disclaimer

Publication types

MeSH terms

LinkOut - more resources