Synthesis of PS and formation of PE in the mitochondrial PSDecarboxylation pathway

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The mechanism by which mitochondrial [[Glycerophosphoserines_(GP03)|PE]] is transported to the plasma membrane is not
The mechanism by which mitochondrial [[Glycerophosphoserines_(GP03)|PE]] is transported to the plasma membrane is not
known, but the process is energy dependent and insensitive to the [http://en.wikipedia.org/wiki/Golgi_apparatus Golgi] disrupting toxin
known, but the process is energy dependent and insensitive to the [http://en.wikipedia.org/wiki/Golgi_apparatus Golgi] disrupting toxin
-
brefeldin A. The results with brefeldin A indicate that the route followed by [[Glycerophosphoserines_(GP03)|PE]] is likely to
+
brefeldin A. The results with brefeldin A indicate that the route followed by [[Glycerophosphoserines_(GP03)|PE]] is likely to bypass the [http://en.wikipedia.org/wiki/Golgi_apparatus Golgi apparatus]. <br> Other pages in this category: <br> <categorytree mode=all hideroot=on>Phospholipid_metabolism</categorytree> <br> <br>
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bypass the [http://en.wikipedia.org/wiki/Golgi_apparatus Golgi apparatus]. <br> Other pages in this category: <br> <categorytree mode=all hideroot=on>Phospholipid_metabolism</categorytree> <br> <br>
+
[[Category:Phospholipid_metabolism]]
[[Category:Phospholipid_metabolism]]

Revision as of 12:13, 20 July 2011

Phosphatidylserine (PS) is formed by the condensation of serine with a phosphatidic acid (PA) moiety, where in mammalian cells phosphatidylcholine (PC) or phosphatidyl ethanolamine (PE) serve as the phosphatidyl donors catalyzed by PS-Synthases (PSS I/II) (Fig. 25 below). Nascent PS is subsequently decarboxylated to form PE, and this reaction is catalyzed by PS-Decarboxylase (PSD) (Fig. 25 below). Both the PS and “Kennedy pathway” are found in mammalian cells but there are some tight restrictions on specific elements of the pathways. In contrast to yeast, the methylation reaction in mammalian cells is not sufficient for supplying all of the PC needed for cell growth. The methylation of PE only occurs quantitatively significant in the liver.
Figure 25.Synthesis and catabolism of phosphatidylserine to phosphatidyethanolamine
In the last years the endoplasmic reticulum and a novel ER-related fraction have been identified as the principal intracellular localization sites of PS-Synthase. The ER-related fraction is tightly associated with the mitochondria and currently referred to as the mitochondria-associated membrane (MAM) compartment (Fig. 26 below). The MAMcompartment can be isolated as a distinct cellular fraction and has significant enrichment in PS-Synthase activity when compared with the total microsomal membrane population. Both morphological and biochemical studies have suggested that the zones of association between the MAM and the mitochondria may also be sites of contact between the outer and inner mitochondrial membrane (Fig. 26 below).
Figure 26. ER and MAM compartment associated PS-metabolism
PS-Decarboxylase was found to be a constituent of the inner mitochondrial membrane and there is a preference for the movement of newly synthesized PS to mitochondria. The PE generated in mitochondria does not only serve as a structural lipid in the mitochondria but is preferentially utilized as a substrate for the methyltransferase reaction to form PC and additionally is exported from mitochondria to function in the biogenesis of other organelles. The mechanism by which mitochondrial PE is transported to the plasma membrane is not known, but the process is energy dependent and insensitive to the Golgi disrupting toxin

brefeldin A. The results with brefeldin A indicate that the route followed by PE is likely to bypass the Golgi apparatus.
Other pages in this category:



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