Martin Johnson

The Chief Medical Officer of Health of the United Kingdom has recommended that the 1990 Human Fertilisation and Embryology Act should be amended to allow cloning in humans for research purposes only. He also recommended that: “The transfer of an embryo created by cell nuclear replacement into the uterus of a woman (so called ‘reproductive cloning’) should remain a criminal offence” (recommendation 7, Ref. 1). This recommendation implies that nuclear replacement and cloning are the same. They are not. Nuclear transfer constitutes reproductive cloning only when the individual created is genetically identical to the nuclear donor. In this paper, we describe a possible future use of nuclear transfer for the treatment of infertile individuals. The treatment yields an individual that receives approximately equal genetic contributions from each parent. We use this example to illustrate how semantic confusion might lead to plausibly moral and justifiable treatments being legally banned. In doing so, we hope to encourage a more accurate and informed use of language in science, law and politics, so that legislation is properly informed by science and achieves what it intends. BioEssays 23:359–364, 2001. © 2001 John Wiley & Sons, Inc.

A major obstacel to the study of mammalian development, and to the practical application of knowledge gained from it in the clinic during therapeutic in vitro fertilisation and embryo transfer (IVF‐ET), is the propensity of embryos to become retarded or arrested during their culture in vitro. The precise developmental cell cycle in which embryos arrest or delay is characteristic for the species and coincides with the earliest period of embryonic gene expression. Much evidence reviewed here implicates free oxygen radicals (FORs) in the process of arrest. Thus, studies on the development of mouse preimplantation embryos in vitro have shown that (i) FORs are elevated in vitro, but not in vivo, at the time at which embryos become arrested or delayed, (ii) systems for removing reactive oxygen species to limit the formation of hydroxy radicals are present, although they have not yet been assessed quantitatively and may differ qualitatively from those in adult cells, (iii) metabolic and possibly genetic adaptations to oxidative damage are evident, (iv) published procedures for overcoming in vitro arrest are explicable in terms of FOR‐mediated damage or responses and (v) the arrest or delay of most embryos in vitro can be reduced or prevented experimentally by addition of metal chelators to limit hydroxy radical formation and lipid hydroperoxidation.

We are each the product of our development. The nature of the developmental process by which each of us was formed is described from gametogenesis to neonatality. The varied influences upon that process and their relative balance and patterns of interaction are then considered. In particular, the relative importance of epigenetic and genetic factors is discussed. It is concluded that development is a continuous process involving epigenetic/genetic interactions throughout. The contemporary emphasis on the genetic basis for human individuality is reviewed critically