Data on inbreeding effects in fishes are impressive, and
<br />include severe body deformities, growth reduction, behav-
<br />ioral changes, and reproductive failures in such forms as
<br />convict cichlids, Cichlosorna nigrofasciatunc (Winemiller and
<br />Taylor 1982), carp, Cyprinus carpio (Moav and Wolfarth 1963,
<br />ref. in Mrakovcic and Haley 1979), zebra fish, Brachydanio
<br />rerio (Mrakovcic and Haley 1979), brook trout, Salvelinus fon-
<br />tinalis (Cooper 1961), and rainbow, trout, Sahno gairdneri
<br />(Aulstad and Kittleson 1971; Gjerde et al. 1983; Kincaid 1983).
<br />Although species and populations differ markedlv in their
<br />resistance to inbreeding depression (Ralls et al. 1979; Frank-
<br />lin 1980), and magnitude of inbreeding effects cannot be
<br />predicted beforehand, "... the unavoidable conclusion is
<br />that relatively small amounts of inbreeding can do tremen-
<br />dous damage to the reproductive potential and productivity
<br />of a fish stock." (FAO/UNEP 1981, p. 10).
<br />A different conservation genetics problem is the imposi-
<br />tion, knowingly or othenvise, of artificial selection upon a
<br />wild stock, leading to a state of domestication (Brisbin 1974).
<br />That fish respond by genetic change to selection in captivity
<br />is well established in salmonids (Vincent 1960; Donaldson
<br />1970; Kincaid et al. 1977) and other groups (Moav et al. 1978;
<br />Hynes et al. 1981). By relaxing natural selection, or replacing
<br />it with random or directional artificial selective forces, the
<br />fate of propagated populations may be jeopardized. Assum-
<br />ing that natural selection has already optimized most char-
<br />acter states of populations in their particular habitats, any
<br />deviation from those states, even those advantageous in
<br />captivity, would not be beneficial in nature. "... genetically
<br />based performance under one set of conditions (i.e., hatch-
<br />ery) may not be correlated with performance under a dif-
<br />ferent set of conditions (stream, lake, natural area). If the
<br />goal is to release stock in a different environment from that
<br />where they are bred, then the brood stock selection practices
<br />must be designed to avoid unconscious selection and in-
<br />breeding." (FAO/UNEP 1981, p. 25).
<br />Frankel and Soule (1981) discuss four types of selection
<br />in captivity that can affect genetics: selection for increased
<br />productivity, selection for a (perfect) type, selection for tract-
<br />ability, and non-selection. Selection for increased produc-
<br />tivity in fishes can occur when the most fecund females are
<br />continually used to develop a breeding stock. Although this
<br />is most efficient in a propagation program,.it can be dele-
<br />terious in nature, where optimal clutch size is a function of
<br />predation risks, growth rates, adult and juvenile mortality
<br />schedules, food availability, etc. (Stearns 1976, 1977). Since
<br />increased fecundity may be maladaptive in nature, this type
<br />of artificial selection should be avoided.
<br />It may also be tempting to select for a particular type, such
<br />as larger or smaller, more or less aggressive, more colorful,
<br />etc. This is analogous to directional or stabilizing selection
<br />and can reduce quantitative or qualitative gene pool varia-
<br />tion. The third type of artificial selection, for tractability, is
<br />really a subset of selection for a type. It occurs when less
<br />aggressive animals are used for breeding because they are
<br />easier to handle. The practice of non-selection occurs when
<br />the survival probability of sick or abnormal individuals is
<br />increased by the captive breeding program; this may in-
<br />crease the incidence of deleterious genes in the population.
<br />Effects of Variance Reduction Within Populations
<br />Thus far, I have presented sources of genetic variance
<br />reduction within populations, under the implicit assump-
<br />tion that loss of variance is undesirable. What specific ge-
<br />netic and phenotypic changes, however, will arise from re-
<br />duced variance, and what is the evidence that these changes
<br />have adverse effects? Loss of genetic variance has three ma-
<br />jor effects: increased homozygosity (leading to reduced fit-
<br />ness), loss of additive variance, and increase in deleterious
<br />recessive alleles.
<br />There is little doubt that increased homozygosity can lower
<br />an individual's fitness (Beardmore 1983) although actual
<br />mechanisms for this reduction are not known. With respect
<br />to relative fitnesses of hetero- and homozygotes, there exists
<br />a "heterozygosity consensus," which is "... the belief based
<br />on extensive laboratory and farm experience that fitness
<br />(variability, vigour, fecundity, fertility, etc.) is enhanced by
<br />heterozygosity, and that any decrease in genetic variation
<br />will be paralleled by a diminution of fitness" (Frankel and
<br />Soule 1981, p. 48). Numerous data sets directly or indirectly
<br />support the notion that reduction in genetic variance may
<br />lower fitness (Wheat et al. 1974; Vrijenhoek and Lerman
<br />1982; Leary et al. 1984) and the interested reader is referred
<br />to Mitton and Grant (1984, and numerous references therein)
<br />for a thorough review. These papers in aggregate demon-
<br />strate that increased homozygosity can result in at least slower
<br />growth, reduced survivorship, and developmental instabil-
<br />ity. Perhaps the most striking example of effects of ho-
<br />mozygosity is in the South African cheetah (Acinonyx j. ju-
<br />batus), which has a paucity of genetic variance at over 200
<br />structural loci and the major histo-compatibility complex,
<br />apparently due to a severe bottleneck (O'Brien et al. 1985).
<br />These animals have great difficulty breeding in captivity,
<br />high rates of juvenile mortality in wild and captive popu-
<br />lations, and an abnormally high susceptibility to an epizootic
<br />coronavirus, all attributed to genetic uniformity.
<br />With respect to the second problem, additive genetic var-
<br />iance is generally lost at the same rate as heterozygosity
<br />1
<br />(2Ne) per generation [Franklin 19k]) . The major cause is
<br />genetic drift, which of course may be powerful in small
<br />populations. The reader is referred to Fisher (1930), Franklin
<br />(1980) and Falconer (1981) for more detailed discussions of
<br />additive genetic variance. The third point, increase in del-
<br />eterious recessive alleles, has been discussed in the section
<br />on inbreeding.
<br />Among-Population Variance
<br />Now we approach a very different problem, that of genetic
<br />variation among populations. Spatially isolated populations
<br />of organisms, with little to no gene flow among them, will
<br />tend to genetically diverge either through different selective
<br />forces or random drift (Endler 1977); in its extreme form,
<br />this leads to speciation. Any isolated population of fishes is
<br />a potentially unique gene pool with characteristics that may
<br />differ from all other demes. This is particularly evident in
<br />salmonids, which demonstrate the potential for extensive
<br />genetic divergence of fish stocks (Donaldson 1971; Busack
<br />et al. 1979; Stahl 1981, 1983). Consequently, in cases where
<br />endangered fishes exist in more than one natural popula-
<br />tion, we have at our disposal a powerful management tool:
<br />the potential existence of genetically distinct groups with
<br />which to recover the species. This is not a trivial observation,
<br />for it allows the manager flexibility in building breeding
<br />stocks, reintroduction to field sites, and other management
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