MAT2A is a protein that synthesizes S-adenosylmethionine (SAM), a methyl donor that is essential for many biological processes. Cellular SAM levels are regulated by a negative feedback loop. When SAM levels are low, the MAT2A transcript is fully spliced, allowing translation of MAT2A protein. When SAM levels are high, an intron is retained, promoting degradation of MAT2A, therefore stopping SAM production. In previous work in Xenopus cells, we observed that MAT2A is downregulated following immune stimulation via poly(I:C), a mimic of viral nucleic acid. The goal of this project is to characterize the regulation of MAT2A in Xenopus laevis, the African clawed frog, following immune stimulation and determine whether SAM and MAT2A level fluctuations post infection are the result of the splicing-related feedback or a metabolic immune response. We transfected X. laevis cells with poly(I:C) and assessed protein levels by Western blotting to determine the earliest point at which MAT2A is downregulated following the immune stimuli. We observed downregulation in the MAT2A proteins six hours post poly(I:C) transfection. We have additionally generated a yellow fever virus replicon to be used instead of poly(I:C) which can potentially shed light on the effects of this metabolic circuit on viral replication and represent a natural infection by an RNA virus more closely. Current investigation is focused on monitoring SAM levels over a time course using immunofluorescence and ELISAs. Preliminary data suggest that SAM levels are reduced following MAT2A downregulation, supporting the idea that this may indeed be a metabolic immune response in Xenopus cells.