11.2.2 The source and nature of genetic variation
Before discussing any further the possible benefits
of genetic diversity, it is worth considering the
question of what is genetic variation? In many stud-
ies on the effect of genetic diversity on population
or community functioning, genetic variation is
taken to be the number of genotypes present. How-
ever, no measure of the degree of genetic dissimi-
larity is given. Although chances are negligible that
two genotypes are exactly identical, that still leaves
a wide range of genetic dissimilarities possible. Ge-
nome-wide screening methods such as amplified
fragment length polymorphisms (AFLPs) or the
use of large numbers of microsatellites or single
nucleotide polymorphisms (SNPs) may give a
more or less reliable measure of overall genetic
diversity because they encompass the entire ge-
nome. Even then, overall genetic diversity in itself
might not be sufficient to enhance population evo-
lutionary potential. Genetic variation matters only
if it translates into phenotypic variation upon
which natural selection can act. If the rise of molec-
ular biology has taught us one thing, it is that the
relationship between genetic and phenotypic diver-
sity is not a straightforward one. Previously, the
most important distinction in genetic variation
was between coding variation and non-coding var-
iation such as neutral markers. Genetic variation in
coding regions leads to amino acid substitutions in
functional proteins, and therefore can contribute to
the relative fitness of the genotype in the popula-
tion. However, the long-held assumption that non-
coding or neutral markers are not part of the pro-
cess of transcription and translation, and hence are
not subject to natural selection, has been challenged
by advances in molecular biology. A much more
complex picture of the molecular genetic organiza-
tion structure now recognizes variation in coding
regions, promoter regions, transcription factor
binding sites, regulatory genes, etc.
The neutral molecular markers often used to
quantify the genetic variability of populations are
at best poorly related to variation in quantitative
traits (Merila and Crnokrak 2001; Reed and Frank-
ham 2001; McKay and Latta 2002). Reed and Frank-
ham (2001) carried out a meta-analysis across 71
studies to determine the mean correlation between
molecular and quantitative measures of genetic
variation. Although molecular measures are com-
monly used as a proxy for quantitative genetic var-
iation, the observed correlation between the two
was weak and not significant (r¼0.217). This anal-
ysis shows the risk in using molecular measures of
genetic diversity to predict population performance
or other population properties, unless there is di-
rect evidence that the markers used are indicative
of the underlying quantitative genetic variation
(Merila and Crnokrak 2001). In all other cases quan-
titative variation is better measured directly.11.2.3 The relationship between genetic and phenotypic diversity
Another reason to apply caution in the extrapola-
tion from genetic diversity to population perfor-
mance is the existence of phenotypic plasticity.
Phenotypic plasticity is the property of a given
genotype to produce different physiological or
morphological phenotypes in response to changing
environmental conditions. Differences in pheno-
typic plasticity can be quantified by measuring a
reaction norm (Viaet al. 1995), which describes the
change in a trait across environments (Fig. 11.2a).
Reaction norms with a steep slope indicate strong
trait sensitivity to the environmental factor, i.e.
strong phenotypic plasticity, whereas a flat reaction
norm denotes weak phenotypic plasticity.
Phenotypic plasticity may account for much of
the phenotypic variation in populations and com-
munities and is thought to play an important role in
adaptation to spatio-temporal heterogeneity in en-
vironmental conditions. Induced phenotypic re-
sponses are a successful conditional strategy to
cope with fluctuating conditions such as tempera-
ture, particularly when there are costs involved in
the induction of the response. For example, the
induction of heat shock proteins protects the organ-
ism from damage through misfolded proteins due
to heat shock exposure. However, there are sub-
stantial energetic and metabolic costs involved,
due to repression of standard cell activity after ex-
posure to heat shock (Krebs and Holbrook 2001).
Constitutive expression of this heat shock response154 FUTURE DIRECTIONS