The temporal separation of macromolecular syntheses from protein assembly into microtubular structures has permitted the use of the Stentor ciliated oral membranellar band regenerating system as an assay for mitotic spindle inhibitors (Banerjee & Margulis, 1971). Melatonin, the pineal gland hormone, is additive to Colcemid in this assay; like Colcemid it specifically inhibits band migration as a sensitive function of developmental stage and concentration. Altho the entire process of band formation and cilia regeneration (stages 0–8) is inhibited by melatonin, stage 3 is especially sensitive.

Delay in morphogenesis at stage 3 can be measured as a precise function of inhibitors (Colcemid, podophyllotoxin, melatonin) of the form y=kxn, where y is delay in hours and k is the concentration of inhibitor in moles. Riboflavin (0.2 μM) and nicotinamide (0.2 μM) in combination reversed Colcemid-induced delay in band regeneration, but (unlike melatonin) the vitamins alone were totally without effect on the regenerating system. Therefore melatonin probably interacts with microtubule protein whereas the B vitamins interact in some way with Colcemid to nullify its activity.