Abstract The exposure of sea urchin eggs and early cleavage stages to bromodeoxyuridine produces consistent abnormalities of development which are identifiable as early as the first blastula stages. It is demonstrated that the BUDR must be available at the time of DNA duplication in order for the effects to be produced, and it is concluded that the abnormalities result from a modification of the DNA itself by substituting BU for thymine. Development is typically abnormal if BU is introduced into the DNA at any time up to the 8-cell stage; the embryos develop into one of two types of persistent abnormal blastulae but do not gastrulate and do not form echinochrome pigments. If the BU is introduced between the 16-cell stage and a ca 100-cell stage, the abnormal blastulae are produced, but echinochrome production is seen. After the ca 100-cell stage, the embryos are relatively insensitive to the BU-substitution. The general observation is that the modification of DNA within very early stages, when it is thought to be inactive in sea urchin development, modifies developmental events whose visible initiation takes place much later.