Abstract
Peroxisomes are ubiquitous, single membrane-bound organelles that play a crucial role in lipid metabolism and human health. While peroxisome number is maintained by the division of existing peroxisomes, nascent peroxisomes can be generated from the endoplasmic reticulum (ER) membrane in yeasts. During formation and proliferation, peroxisomes maintain membrane contacts with the ER. In addition to the ER, contacts between peroxisomes and other organelles such as lipid droplets, mitochondria, vacuole, and plasma membrane have been reported. These membrane contact sites (MCS) are dynamic and important for cellular function. This review focuses on the recent developments in peroxisome biogenesis and the functional importance of peroxisomal MCS in yeasts.
Highlights
Peroxisomes are conserved and highly dynamic organelles that are required for several metabolic processes, including beta-oxidation of fatty acids, reduction of reactive oxygen species, biosynthesis of plasmalogens and bile acids, oxidation of D-amino acids, and synthesis of precursors of cholesterol (Farré et al, 2019)
In Saccharomyces cerevisiae, Yarrowia lipolytica, and Komagataella phaffii, peroxisomes proliferate when grown in fatty acids such as oleic acid, whereas in Ogataea polymorpha and K. phaffii peroxisomes proliferate when grown in methanol (Kunau and Hartig, 1992; Singh et al, 2020)
When yeast cells are grown in fatty acid–enriched growth medium, several other organelles such as the endoplasmic reticulum (ER) and mitochondria are tightly associated with peroxisomes and lipid droplets (LDs) (Sargsyan and Thoms, 2020)
Summary
Peroxisomes are conserved and highly dynamic organelles that are required for several metabolic processes, including beta-oxidation of fatty acids, reduction of reactive oxygen species, biosynthesis of plasmalogens and bile acids, oxidation of D-amino acids, and synthesis of precursors of cholesterol (Farré et al, 2019). Peroxisomes and Membrane Contact Sites biogenesis, addressing the importance of MCS in the formation and function of peroxisomes in yeasts. Deletion of OpPex24 and OpPex32 leads to defects in peroxisomal matrix protein import, membrane growth, and peroxisome proliferation, possibly due to defects in peroxisome–ER contact.
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