To identify those mechanisms, Scripps microbiologist Ben Shen and his colleagues performed bioinformatics analyses of the open reading frames in the genomes of two strains of S. platensis and identified four genes that, based on their homology to enzymes of known function and their apparent lack of a role in antibiotic biosynthesis, the researchers hypothesized may confer resistance to platensimycin and platencin. Follow-up experiments revealed that the enzyme PtmP3, which is resistant to the antibiotics, had replaced two fatty acid biosynthesis enzymes, FabF and FabH, which are normally inhibited by the compounds, and expression of PtmP3 in the normally susceptible S. albus rendered the bacteria resistant to both antibiotics. Moreover, S. platensis’s FabF had evolved structural changes so as to be resistant to platensimycin, serving as “a second form of self-resistance,” the authors wrote.