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Our recognition of the mitochondria as being important sites of fatty acid biosynthesis is continuously unfolding, especially in light of new data becoming available on compromised fatty acid synthase type 2 (FASII) in mammals. For example, perturbed regulation of murine  17β-HSD8  encoding a component of the mitochondrial FASII enzyme 3-oxoacyl-thioester reductase is implicated in polycystic kidney disease. In addition, over-expression in mice of the  Mecr  gene coding for 2- trans -enoyl-thioester reductase, also of mitochondrial FASII, leads to impaired heart function. However, mouse knockouts for mitochondrial FASII have hitherto not been reported and, hence, there is a need to develop alternate metazoan models such as nematodes or fruit flies. Here, the identification of  Caenorhabditis elegans  W09H1.5/MECR-1 as a 2- trans -enoyl-thioester reductase of mitochondrial FASII is reported. To identify MECR-1,  Saccharomyces cerevisiae etr1 Δ mutant cells were employed that are devoid of mitochondrial 2- trans -enoyl-thioester reductase Etr1p. These yeast mutants fail to synthesize sufficient levels of lipoic acid or form cytochrome complexes, and cannot respire or grow on non-fermentable carbon sources. A mutant yeast strain ectopically expressing nematode  mecr-1  was shown to contain reductase activity and resemble the self-complemented mutant strain for these phenotype characteristics. Since MECR-1 was not intentionally targeted for compartmentalization using a yeast mitochondrial leader sequence, this inferred that the protein represented a physiologically functional mitochondrial 2- trans -enoyl-thioester reductase. In accordance with published findings, RNAi-mediated knockdown of  mecr-1  in  C. elegans  resulted in life span extension, presumably due to mitochondrial dysfunction. Moreover, old  mecr-1(RNAi)  worms had better internal organ appearance and were more mobile than control worms, indicating a reduced physiological age. This is the first report on RNAi work dedicated specifically to curtailing mitochondrial FASII in metazoans. The availability of affected survivors will help to position  C. elegans  as an excellent model for future pursuits in the emerging field of mitochondrial FASII research.

A C. elegans Model for Mitochondrial Fatty Acid Synthase II: The Longevity-Associated Gene W09H1.5/mecr-1 Encodes a 2-trans-Enoyl-Thioester Reductase