Biotin requirements are lower in human Jurkat lymphoid cells but homeostatic mechanisms are similar to those of HepG2 liver cells.

The following proteins are candidates for maintaining biotin homeostasis in humans: the biotin transporters sodium-dependent multivitamin transporter (SMVT) and monocarboxylate transporter 1, the biotinyl-protein ligase holocarboxylase synthetase (HCS), and the lysine-epsilon-biotin hydrolase biotinidase. Liver cells are supplied through the portal vein with high levels of water-soluble vitamins compared with those of peripheral tissues. We hypothesized that the mechanisms of biotin homeostasis are qualitatively and quantitatively different in cells derived from human liver (HepG2 cells) and lymphoid tissues (Jurkat cells). Cells were cultured in biotin-defined media, representing deficient (D), normal (N), and supplemented (S) individuals. Biotinylation of carboxylases depended on biotin availability in both cell types, but HepG2 cells required 3 times more biotin than Jurkat cells to maintain normal levels of holocarboxylases. The expression of biotin transporters was less in both types in medium S compared with cells in media D and N; in contrast, the expression of HCS was higher in cells in medium S compared with the other cells. The abundance of 3-methylcrotonyl-CoA carboxylase mRNA was lower in cells in medium D than cells in media N and S. The enrichment of biotinylated histones was higher at the SMVT promoter 1 in HepG2 and Jurkat cells in medium S compared with the corresponding cells in media D and N, presumably repressing the SMVT gene. The mechanisms of biotin homeostasis are qualitatively similar but quantitatively different in HepG2 and Jurkat cells; HCS, histone biotinylation, and biotin transporters play a role in homeostasis in both.