To the editor:

While reading about developmental defects and high rates of mortality among animals produced by cloning (Nature Biotechnology 17, 405, 1999), we were reminded of similar problems encountered by plant scientists when cloning plants from cultured somatic cells. Considerable phenotypic variability has been observed among presumably genetically identical plants regenerated from cell or tissue culture, a phenomenon that has been called somaclonal variation1. Although the basis of somaclonal variation remains unclear, a substantial epigenetic component has been proposed2,3. In particular, developmentally acquired epigenetic states, which would normally be reset during sexual reproduction, can be stably maintained during regeneration of plants from somatic cells, resulting in the silencing of genes that normally would be expressed3.

Some of the abnormalities and deaths of cloned mammals might relate to disruptions in the epigenetic phenomenon of parental imprinting. However, imprinting disturbances probably do not account for all of the problems in cloning4, possibly implicating more general epigenetic alterations involving nonimprinted genes. Whatever proves to be the source of abnormalities in cloned animals, a lesson from plants is that "clonal uniformity is the exception rather than the rule"5.