What's killing the cheetah?

Genetic bottlenecks severely alter how a population is able to respond to its environment; bottlenecks drastically reduce size in populations and lead to inbreeding and the massive consequences associated with it. Why is inbreeding bad? Genetic theory predicts inbreeding will reveal deleterious recessive alleles which may be manifested later in lowered fecundity, high infant mortality and reduced growth rate. In situations where it is common, probability of extinction is increased and opportunities for evolution are limited. (Ecological)

It is essential then that we identify the above symptoms in populations of concerned species. Ten thousand years ago cheetahs underwent a genetic bottleneck. By conjecture, it lacked genetic variability. Ecologists began studying the cheetah in captivity, reporting deleterious recessive alleles, consistent with low genetic diversity, as a cause for its poor fecundity. Recent observations, however, have been conducted in the wild, and are designed to literally watch the hand of genetic theory snatching cubs from the lair. What did these studies find? Well, in “Ecological and Genetic Factors in Conservation: A Cautionary Tale”, lions not lack of heterozygosity are being blamed for the cheetahs decline.

First, do populations of cheetah actually lack genetic variability? The answer is yes; there is no doubt the cheetah lacks genetic variability- Individuals in populations almost all can be considered brother and sister. How do we know? The major histocompatibility complex (MHC) is a multigene complex of homologous genes that encode antigens that play a key role in immune response. In most species, MHC gene products display extreme polymorphism- their variability interpreted as an adaptive strategy for accommodating rapidly evolving infectious agents that periodically afflict natural populations. By observing a gene known to be highly polymorphic among individuals in populations thought to be genetically depauperate, we are able to observe percent polymorphism for a gene over that population and directly determine presence or lack of polymorphism. Such was the basis for the study “DNA Variation of the Mammalian Major Histocompatibility Complex Reflects Genomic Diversity and Population History.” In it, N Yuhki et al calculate and compare percent polymorphism in individuals of South African and East African cheetahs. Their quantitative analysis of the genes supported previous qualitative analysis where skin grafts between 12 unrelated and 2 sibling cheetahs all failed to be rejected acutely, suggesting lack of genetic variability. (MHC)

Until recently the Cheetah has categorically realized predictions of genetic theory. The cheetah lacks genetic variability and its ability to respond to the environment and disease has been reduced. But does reduced genetic variability really account for reduced fecundity? In “Captive Breeding of Cheetahs in North American Zoos: 1987-1991,” Kraus et al quantify the results of attempts across North America to breed the cheetah in captivity. For cubs born to related parents (inbred) of southern African origin, the frequency of mortality was 14 of 34, or 41 %. By comparison, the mortality frequency for cubs born to related parents of East/southern African hybrid parents was 15 of 37, or 41 %. By contrast, the frequency for cubs born to unrelated parents (non-inbred) from southern African origin was 22 of 89, or 25%, and for cubs born from unrelated hybrid parents of East/southern African origin, 6 of 41, or 15%. In their study, outbreeding resulted in infant mortality rates that clearly followed a pattern where as genetic dissimilarity in parents increased, infant mortality in offspring decreased. Clearly, fecundity is linked to genetic variability. (Captive)

T.M. Caro et al refused to believe this was the case in the wild. In “Ecological and Genetic Factors in Conservation: A Cautionary Tale,” they tracked the timing of births and locations of lairs. Soon after a female had given birth, they entered lairs to count and weigh the cubs while the mother was known to be away hunting. Of the 125 cubs given birth to, 36 survived and infant mortality was calculated to be a high 80%. It looked as if the wild cheetah too could not escape predictions of genetic theory. However, their study was furthered as next, they sought to directly observe the cubs at their time of death. Observers were shocked. Lions were often caught preying upon entire litters of cubs. Caro writes, “Lions accounted for infant mortality in 35.5 out of 48.5 deaths”. Caro's data offers new explanation for the plight of the cheetah. Moreover, high numbers of females breeding and rapid rates of litter production are implying that neither the reproductive anatomy or physiology of either sex is functionally compromised as a result of genetic monomorphism- this, coupled with the data above, is leaving many wondering whether genetics is being overemphasized in relation to the plight of the cheetah. (Ecological)

Lack of heterozygosity can theoretically affect juvenile mortality. However, data gathered in the wild, taken directly from the lair, show rates of mortality can't be explained primarily by genetic problems. It seems ill-advised to continue to cite the cheetah as a species suffering from a consequence of low genetic diversity. (Extrinsic Factors)

In the wild, the cheetah is not bound by assumptions in theories.




Posted by: John