6.3.1.21	E217A	the mutant loses its ATP-binding capability	-, 756596	
6.3.1.21	G162I	site-directed mutagenesis, the enzyme mutant releases formyl phosphate into solution, reduced activity compared to wild-type enzyme	760556	
6.3.1.21	additional information	isolation of mutants defective in GAR transformylase activity, generation of single and double null mutants of genes purT and purN, phenotypes, overview	761366	
6.3.1.21	additional information	single mutants of Salmonella enterica serovar Typhimurium strain 4/74 are created by deletion of the purN and purT genes, generation of different purT (encoding formyltetrahydrofolate deformylase, EC 3.5.1.10) and purU mutants. The DELTApurU/DELTApurT mutant shows increased virulence in macophages compared to wild-type, while all other mutants have reduced virulence. purN and purT mutants grow somewhat slower than the wild-type. Mutation of purN but not purT attenuates the strain during interaction with cultured macrophages. Single-gene deletions of each of the purT and purN causes in mouse infections. While the DELTApurT mutant multiplies as fast as the wild-type strain in cultured J774A.1 macrophages, net multiplication of the DELTApurN mutant is reduced approximately 50% in 20 h. The attenuation of the DELTApurT mutant is abolished by simultaneous removal of the enzyme PurU, responsible for the formation of formate, indicating that the attenuation is related to formate accumulation or wasteful consumption of formyl tetrahydrofolate by PurU	-, 761243	
6.3.1.21	R131A	the mutant loses its ATP-binding capability	-, 756596	
6.3.1.21	S218A	the mutant loses its ATP-binding capability	-, 756596	
6.3.1.21	V220A	the mutant loses its ATP-binding capability	-, 756596