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Humans and many other organisms express multiple SAM synthases. However, loss of different synthase activity can have distinct phenotypic effects. For instance, in\n                    <jats:italic>Caenorhabditis elegans<\/jats:italic>\n                    loss of\n                    <jats:italic>sams-1<\/jats:italic>\n                    leads to enhanced heat shock survival and increased life span, but loss of\n                    <jats:italic>sams-4<\/jats:italic>\n                    reduces heat stress survival. This provides a biological context to test the hypothesis that the enzymatic source of SAM impacts its function and to identify mechanistic connections. Here, we show that SAMS-1 contributes SAM to a variety of intermediary metabolic pathways, whereas SAMS-4 has a more limited role to support SAM-dependent protein transmethylation reactions. Mitochondria seem to be particularly impacted specifically by loss of\n                    <jats:italic>sams-1<\/jats:italic>\n                    ; many mitochondrial metabolites are perturbed and there is an age-dependent decline of nuclear-encoded mitochondrial gene expression in these animals. We further demonstrate that reduced production of phosphatidylcholine in\n                    <jats:italic>sams-1<\/jats:italic>\n                    -deficient animals leads to mitochondrial fragmentation and subsequent loss of mitochondrial components. 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