Sphingolipids are vital components of cellular membranes and perform a wide range of essential biological functions. They are derived from sphingosine, which undergoes N-acylation to form ceramide, the foundational building block for sphingomyelin and glycosphingolipids. Beyond serving as precursors for complex sphingolipids, sphingosine and ceramide are also key players in cellular signaling. Sphingosine can be phosphorylated by sphingosine kinases to generate sphingosine-1-phosphate, a potent signaling molecule involved in processes like cell proliferation and survival. Conversely, the upregulation of ceramide levels and its localization to mitochondria, can trigger apoptotic cell death. However, studying the direct mechanisms by which these sphingolipid intermediates exert their signaling functions is challenging due to their short-lived nature and the highly interconnected sphingolipid biosynthetic network. When this network is targeted, e.g. by genetic ablations in lipid metabolic enzymes, this may cause its rewiring and dampen the biological impact. As a result, chemical approaches have become increasingly important for investigating lipid metabolism and signaling. One such approach involves the use of photocaged lipids, where a photolabile group, or photocage, is attached to the headgroup of the lipid, masking its biological activity. Additionally, a terminal alkyne is introduced for detection. Upon exposure to UV light, the photocage is cleaved, releasing the bioactive lipid. To increase spatial precision, the photocage can be coupled to organellar targeting moieties, causing the lipid to accumulate in specific subcellular compartments. We developed photocaged variants of sphingosine targeted to the endoplasmic reticulum (ER) and ceramide targeted to the mitochondria. Our studies demonstrated that these caged lipid probes accumulate in their respective target organelles and remain metabolically and biologically inert. Upon UV light exposure, we observed efficient metabolic incorporation of the ER-targeted sphingosine into the cellular lipid pool. On the other hand, photorelease of ceramides in mitochondria triggered Caspase-9 dependent apoptosis, highlighting the precise control of lipid activity and its compartment specific impact on cellular processes. In addition to photocaged compounds we also created photoswitchable sphingosines and ceramides. These molecules contain a photosensitive azobenzene group in their hydrocarbon chain, which can be reversibly switched between its straight trans- and bent cis-conformation upon exposure to light. We demonstrated via TLC- and mass-spectrometry analysis that both in vitro and in vivo they serve as light-sensitive substrates for various enzymes within the sphingolipid biosynthetic network. Counterintuitively, the bent cis-isoform of both ceramide and sphingosine serves as the preferred substrate for the sphingolipid metabolic machinery compared to the straight trans isoform. The metabolic conversion of these compounds can be reversibly controlled by exposure to UV or blue light, enabling precise temporal regulation and dynamic manipulation of their incorporation into the endogenous sphingolipid pool. Taken together, we have developed a diverse toolbox of photocaged and photoswitchable sphingolipid precursors, which can be used to acutely manipulate sphingolipid metabolism and signaling, and furthermore can be used to provide new insights into the compartment-specific functions of these lipid species.