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Intl. J. of Mol. Ecol. and Conserv. 2012, Vol. 2, No.1, 1-7
http://ijmec.sophiapublisher.com
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specimens, the kestrel lost about 50% of
heterozygosity on microsatellites during the
bottleneck (Groombridge et al., 2000), however,
Amos and Balmford (2001) comments that this was an
exceptional case where a high percentage of
heterozygosity was lost. Furthermore, data from the
Antarctic fur seal (
Arctocephalus gazelle
) indicate that
extreme but short-term depletion may have little
impact on heterozygosity as this species shows little
evidence of genetic erosion after severe depletion by
sealers (Gemmell et al., 2001). Genetic drift is a long
term threat, conclusions from short-term studies might be
biased because of lack of long-term data and projections
from models might over-estimate the risk of extinction.
The more important the genetic variability (in terms of
both absolute selective value and the proportion of
time any advantage is manifest), the more likely it
would be to be retained in a species` population
(Amos and Balmford, 2001). Most of the genetic
variance responsible for an evolutionary response to
natural selection (the additive genetic variation) is
found in high-frequency alleles, those least likely to
be lost in small populations (Poon and Otto, 2000).
Hence drift tends preferentially to remove the
variability which is currently least important to the
organism; implying that the population will under
immediate threat of extinction, although consequences
in the long-term will be uncertain.
Genetic variation lost during a bottleneck is a function
of growth rate (Nei et al., 1975). Little variation will
be lost in species that quickly recover and have long
overlapping generations (reproduce many times
therefore variability present in a cohort is likely to be
transferred to future generations) (Gaggiotti and
Vetter, 1999). Species that have gone through
bottlenecks (e.g. California sea otter and Indian
rhinoceros) do not necessarily show reduced genetic
variation, but in those that do, the number of
deleterious recessives depends on the rate of
bottleneck occurrence; if rate was slow they would
have been purged but not fixed (Caro and Laurenson,
1994). This means if rapid population declines are
quickly corrected then little genetic variation
especially in long-lived species.
The loss of allelic diversity can have serious
consequences in the short term if it occurs at loci
associated with disease resistance such as the major
histocompatibility complex (MHC) in vertebrates
(Allendorf and Ryman, 2002). Low variation at the
MHC complex after bottlenecks has extinction risks
for example in the Arabian oryx (
Oryx leucoryx
). A
study of this species reported only 3 alleles at the
MHC class II DRB from 57 individuals (Hedrick and
Kim, 2000). It went extinct in the wild in 1972
(because of hunting) and captive populations were
vulnerable to tuberculosis and foot and mouth diseases.
However, cross-species comparisons are ambiguous as
the Northern elephant seal (
Mirounga angustirostris
)
show low MHC diversity but is not prone to a range of
diseases compared to Californian sea lions (
Zalophus
californianus
) that use the same habitats (Hoelzel et al.,
1993). Low MHC variability therefore is a serious risk
but cannot be set as a rule for all species as some only
show negative effects when there are other confounding
factors such as reduced effective population size (
N
e
),
limited resources and predation.
Few species populations have been reported to have
gone extinct or decline primarily due to loss of
heterozygosity (Caro and Laurenson, 1994). The
cheetah (
Acinonyx jubatus
) is commonly cited as
lacking genetic variation and this was previously
blamed for its poor survival prospects in the wild. In
the mid 1980s, a study of 55 cheetahs from southern
Africa demonstrated complete lack of variation at
each of 47 allozyme loci (O'Brien et al., 1985), skin
grafts were not rejected among animals implying that
their immune systems were genetically identical.
Further studies in 1990s questioned whether wild
cheetah’s survival was being compromised by their
lack of genetic variation, and Caro and Laurenson
(1994) pointed out that disease susceptibility and
breeding problems were an issue more for captive
cheetahs while predation was more important in the
wild population. The claims that cheetah lost 90-99%
of its variability in one or more bottlenecks (O'Brien,
1994) are questionable as it would require 16
generations of sib-sib mating (
N
e
=2) to lose 99% of
genetic variation (Amos and Balmford, 2001). A
recent study in Namibia (Castro-Prieto et al., 2011)