In cultured mammalian cells disruption of ATP citrate lyase, an enzyme that supplies nucleocytoplasmic acetyl CoA. Conversely, reduced expression of acetyl CoA carboxylase 1, a cytosolic enzyme that competes with HATs for nucleocytoplasmic acetyl CoA, caused an increase in bulk histone acetylation. Moreover, a surge in intracellular acetyl CoA during the oxidative phase of yeast metabolic cycles induced the Gcn5p/SAGA-catalysed acetylation of histones at growth genes and acted as a trigger for initiating a cellular growth programme and cell cycle entry. Intracellular acetyl CoA levels have also been implicated in regulation of Na-linked acetylation and apoptosis. Overexpression of Bcl-xL in human cells caused a reduction in cellular acetyl CoA and a concomitant decrease in protein Na-acetylation, which could be restored by increasing acetyl CoA levels by addition of citrate or acetate. High levels of acetyl CoA and Na-acetylation were shown to be associated with increased susceptibility to apoptotic stimuli. Considering the emerging role of intracellular acetyl CoA levels in the regulation of cell growth, differentiation, cell cycle, and apoptosis, we sought to measure changes in the level of this metabolite in vivo during the embryonic development of a vertebrate. Most in vivo measurements of CoA species have been limited to tissues of adult organisms subjected to different conditions, whereas how the levels of CoA species change in a developing organism is largely unknown. In this study we used embryos of Xenopus laevis, a widely used model species for studying cellular processes underlying embryogenesis. In the present study, we have used Xenopus laevis as a model organism to measure changes in whole-embryo levels of CoA and acetyl CoA in vivo during vertebrate embryonic development. As far as we are aware, the only other study that has measured acetyl CoA levels during the early embryonic development is that by Vastag et al, who employed a mass spectrometry based approach to measure changes in 48 common metabolites, including acetyl CoA, during early Xenopus embryonic development. Based on their data they concluded that there is no observable change in acetyl CoA levels between fertilisation and 11 h post-fertilisation. This contradicts our data showing a small but statistically significant increase in acetyl CoA levels between stage 4 and stage 8/9. The discrepancy may be explained by the different approaches used by the two studies for sampling and data analysis. Vastag et al measured metabolites in each of 10– 11 individual embryos, obtained from three different clutches of eggs, at five different stages between fertilisation and stage 9. Data from individual embryos were then analysed and presented separately. This approach was used to identify metabolites whose concentrations change robustly and consistently in every embryo.