regions of the fish with this atypical phenotype becomes progressively more severe and reduces viability. Further, all F1 progeny were deformed seriously, with excessive cartilage growth in the cranium, operculum, and lower jaw, and they had low viability. The deformities in the offspring were more severe than those observed in their parents at the same age. Devlin attributed this to the mosaicism between founder and F1 generation, with elevated levels produced in the F1. Devlin et al. (1995a) concluded that the best optimal long-term stimulation is achieved in transgenic individuals that show intermediate levels of initial growth enhancement.

As in mice, the genetic background of particular selected strains of farm animals probably is important in determining the severity of the defects associated with the transgene. Pursel et al. (1989) speculated that the deformities found in the Beltsville pigs would have been less severe if the foundation stock had been selected for leg soundness and adaptation to commercial rearing conditions.


Because there can be so much variation in the sites of gene insertion, the numbers of gene copies transferred, and the level of gene expression (Chapter 2), every transgenic animal produced by microinjection is (theoretically, at least) unique in terms of its phenotype. Pigs transgenic for growth hormone, for example, vary enormously in the number of DNA copies that they have per cell (from 1 to 490) and in the amount of growth hormone that they secrete (from 3 to 949 nanograms per milliliter, or ng/ml). Half of pigs transgenic for a gene (c-ski) intended to enhance muscle development experienced muscle weakness in their front legs, and in general the degree and site of muscle abnormality in these pigs varied considerably from one individual to another (Pursel et al., 1992).

This variability makes the task of evaluating the welfare of transgenic animals particularly difficult, since adverse effects almost are impossible to predict in advance, and each individual animal must be assessed for such effects. Van Reenen and Blokhuis (1993) describe the difficulties involved in such assessments. In most cases, deleterious phenotypic changes in transgenic farm animals—particularly animals transgenic for growth hormone or other growth promoting factors—have been easy to detect because they cause such gross pathologies. However, more subtle effects also are possible. Growth hormone, for example, has many systemic effects, including effects on the efficiency of nutrient absorption, fecundity, and sexual maturation (Bird et al., 1994). Growth hormone constructs in salmonids have been shown to influence smoltification (Saunders et al., 1998), gill irrigation, disease resistance, body morphometry (Devlin et al., 1995a,b), pituitary gland structure (Mori and Devlin, 1999), life

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