May 30, 2011 Peroxisomes are cell organelles that can cause disease and aging processes if they do not function properly. For the first time ever, University of Groningen researchers have demonstrated that peroxisomes can be created by two independent processes, one of which serves as a kind of 'backup'. The study was published in the 23 May issue of the Journal of Cell Biology.
Peroxisomes are cell organelles that play an important role in hydrogen peroxide and fatty acid metabolism. Impaired peroxisome function can lead to serious diseases and contributes to aging processes.
Lack of clarity
Two mechanisms by which peroxisomes proliferate are known: division of an existing peroxisome and creation of a new one by budding from another cell organelle, the endoplasmic reticulum (ER). There is a lack of clarity in scientific circles regarding the status of the two mechanisms.
Independent after all
In their Journal of Cell Biology article, the Groningen researchers are the first to describe the proteins which are essential in creating peroxisomes from the ER. This discovery was subsequently used to inhibit the formation of these proteins. It transpired that when ER peroxisome production ceased, this had little or no effect on the numbers of peroxisomes present in the cell. This proved that peroxisomes are indeed independent cell organelles capable of proliferation by division, just like other important cell organelles such as mitochondria.
Formation of organelles from the ER is probably an important backup mechanism when a cell has lost all its peroxisomes. In that case, peroxisomes can be created de novo in a cell. These results are a major contribution to the debate on the importance of the ER peroxisome formation process.
Other social bookmarking and sharing tools:
Note: Materials may be edited for content and length. For further information, please contact the source cited above.
- R. Saraya, A. M. Krikken, M. Veenhuis, I. J. van der Klei. Peroxisome reintroduction in Hansenula polymorpha requires Pex25 and Rho1. The Journal of Cell Biology, 2011; DOI: 10.1083/jcb.201012083
Note: If no author is given, the source is cited instead.