Chick embryo fibroblasts cease to synthesize their normal collagen product when grown in the presence of the thymidine analogue, 5-bromodeoxyuridine (BrdU). The drug causes an alteration of synthesis from the normal Type I collagen (alpha1 (I)2alpha2) to a mixture of Type I and Type I trimer (alpha1(I)3). While the significance of the synthesis of Type I trimer is unclear, it has been noted that chondrocytes synthesize this collagen type following in vitro senescence and in the presence of BrdU. Since BrdU may cause a switching in the temporal pattern of collagen biosynthesis in chondrocytes and in fibroblasts it is proposed that BrdU may alter the normal regulatory controls acquired by the cells during the course of their differentiation. The synthesis of type I trimer might provide a marker for such a break-down in a wide variety of cell types.