Involved in the flower biosynthesis of vindoline, a precursor of vinblastine and vincristine (PubMed:10481044, PubMed:12228585, PubMed:24108213). Hydroxylates specifically tabersonine, 2,3-dihydrotabersonine and 2,3-dihydro-3-hydroxytabersonine, but has no activity with naringenin, tryptamine, secologanin, strictosidine, ajmalicine, vindoline and catharanthine (PubMed:24108213). (-)-tabersonine + O2 + reduced [NADPH--hemoprotein reductase] = 16-hydroxytabersonine + H(+) + H2O + oxidized [NADPH--hemoprotein reductase] concentrations of tabersonine greater than 30 uM are inhibitory. Optimum pH is 7.5 in phosphate buffer and 8.0 in TRIS-HCl. Stable at 30 degrees Celsius. Alkaloid biosynthesis; vindoline biosynthesis. The ER localization is dependent on the presence of the putative transmembrane helix. Predominantly expressed in young leaves of mature plants (PubMed:12228585, PubMed:16262708). Low expression in roots and flowers, but not detected in stems and old leaves (PubMed:12228585, PubMed:16262708). Found predominantly in leaf epidermis (PubMed:12228585, PubMed:16262708). Barely detected in roots, internodes, young and mature leaves, and flower buds, but relatively abundant in fully developped flowers (PubMed:24108213). Not detected in leaf epidermal cells (PubMed:24108213). Peak of expression after light treatment at 9 days of seedling development. Up-regulated by methyl jasmonate (PubMed:24108213). Inhibited by cytochrome c, CO, clotrimazole, miconazole, tricliphane, flusilazole and tetcyclasis, and with a lower efficiency, by 1-phenylimidazole and piperonylbutoxide. Not inhibited by potassium cyanide and sodium azide. Tabersonine 16-hydroxylation is orchestrated in an organ-dependent manner by two genes including CYP71D351, which encodes the T16H2 isoform acting in the foliar vindoline biosynthesis, and CYP71D12, which encodes the T16H1 isoform acting in the flower vindoline biosynthesis. Belongs to the cytochrome P450 family.