Abstract
Cell division in zygotes of the sand dollar, Echinarachnius parma, is delayed by ultraviolet (UV) irradiation. UV-sensitivity is enhanced 2–3-fold after incorporation of 5′-bromodeoxyuridine (BUdR) into DNA; photoreactivability in such zygotes is greatly diminished or absent. These observations support the hypothesis that DNA is the responsible light absorber in UV-induced cell division delay. The pattern of onset of hypersensitivity to UV indicates that delay in a given cleavage is the result of lesions in the DNA which has not been replicated in the S period prior to that cleavage; lesions formed in DNA which, at the time of irradiation, has already been replicated, are not expressed until the subsequent cell division. UV does not prolong the UV-sensitive portion of the cell cycle. This result implies that delay in (sensitive) DNA replication per se is not part of the overall mechanism of division delay.
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