Involved in pyrimidine catabolism (PubMed:16540542). Catalyzes the deamination of 3-aminoacrylate to malonic semialdehyde, a reaction that can also occur spontaneously (PubMed:33839153). RutC may facilitate the reaction and modulate the metabolic fitness, rather than catalyzing essential functions (PubMed:33839153). In vitro, can also deaminate 2-aminoacrylate (PubMed:33839153). (Z)-3-aminoacrylate + H(+) + H2O = 3-oxopropanoate + NH4(+) kcat is 52 min(-1) with 3-aminoacrylate as substrate. Homotrimer. Up-regulated by the nitrogen regulatory protein C (NtrC also called GlnG) and repressed by RutR. Cells lacking this gene fail to grow on uridine as the sole source of nitrogen at room temperature (PubMed:20400551, PubMed:33839153). Expression of rutC in trans did not restore growth (PubMed:33839153). However, a plasmid carrying the complete rutCDEFG operon restored growth of the deletion mutant with uridine as sole nitrogen source, suggesting that the lesion in rutC was polar on downstream gene(s) required for rut pathway function (PubMed:33839153). This reaction can occur spontaneously. Under standard laboratory conditions, a Rut pathway lacking RutC generates sufficient nitrogen from uracil for growth of E.coli. The Rut pathway degrades exogenous pyrimidines as the sole nitrogen source at room temperature but not at 37 degrees Celsius, a restriction that is apparently a consequence of an inadequate ability to remove toxic malonic semialdehyde at the higher temperature (RutE/YdfG function). Belongs to the RutC family.