Texas A&M University: GENETIC DIVERSITY OF WHITE TIGERS AND GENETIC FACTORS RELATED TO COAT COLOR

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GENETIC DIVERSITY OF WHITE TIGERS AND GENETIC

FACTORS RELATED TO COAT COLOR
Approved by:
Research Advisor: Dr. Jan Janecka
Major: Biomedical Sciences
Wildlife and Fisheries Sciences
May 2013
Submitted to Honors and Undergraduate Research
Texas A&M University

ABSTRACT
Genetic Diversity of White Tigers and Genetic Factors Related to Coat Color. (May 2013)
Sara Elizabeth Carney
Department of Veterinary Medicine and Biomedical Sciences
Texas A&M University
Research Advisor: Dr. Jan Janecka
Department of Veterinary Medicine and Biomedical Sciences
White tigers are greatly cherished by the public, making them valuable to zoos and breeders.
Unfortunately, a number of health issues have occasionally surfaced within some of the white
tiger population such as neurological and facial defects. There is interest amongst private tiger
breeders to determine if these maladies are associated with the coat color or breeding practices,
and to find ways to prevent these health issues. The genes involved in producing the white
phenotype and the disease phenotype are currently unknown. Furthermore, the relationship
between the genes associated with coat color and levels of inbreeding also remain unknown.

INTRODUCTION
To many the white tiger, Panthera tigris, has been a source of awe, combining the power and
grace exhibited by the standard orange tiger with the rare beauty from its unusual coat color.
Though many find the white tiger to be inspiring, this is not a universally held opinion. Critics
contend that the white tiger is a detriment to tiger conservation, claiming that the tigers must be
inbred in order for the white coat to be present. Furthermore, they attribute the ailments faced by
some white tigers (eg. crossed-eyes and cleft palates) (Roychoudhury and Sankhala 1978) to the
white coat trait, believing it to be inseparable from inbreeding.
In light of this controversy, it is important to determine the white tiger’s role in conservation of
the species. Though some do not place priority on the preservation of the white tiger, it is evident
that the species as a whole is facing the threat of extinction. Three of the original eight tiger
subspecies, Bali (Panthera tigris balica), Caspian, (Panthera tigris virgata), and Javan
(Panthera tigris sondaica), have recently become extinct (Luo et al. 2004). The tiger population
has faced recent rapid decline. Within the last 100 years the wild tiger’s habitat has been reduced
to only 7% of the land in once roamed (Dinerstein et al. 2007). Poaching as well as habitat loss
and fragmentation poses the greatest threat to the wild tiger population. Deforestation has
significantly impacted the wildlife present in these areas particularly the tiger and its prey
(Kinnaird et al. 2003). The tiger faces additional risks associated with its dwindling population,
primarily decreased genetic diversity. Frequently, populations facing significant decline may
resort to inbreeding, potentially leading to inbreeding depression (Hedrick and Kalinowski
2000). Consequently, deleterious homozygotic traits that were once masked in a healthy population of heterozygotes may become rampant in a genetically isolated population. Thus, this
genetically compromised population becomes increasingly vulnerable to disease (Lynch 1977).
While the wild tiger population faces steady decline, the captive population has successfully
propagated. Tigers have relatively few complications associated with reproduction, which often
plagues captive breeding programs. Additionally, captive-bred populations are protected from
many of the threats that face their wild counterparts, such as habitat degradation, disease and
poaching. Though the captive tiger has escaped many of these issues, loss of genetic diversity is
still a present concern within segments of the population (Lacy 1987). The white tiger is
particularly vulnerable to increased homozygosity due to selection for this phenotype. In many
ways the captive environment has allowed rare coat color polymorphisms such as that of the
white tiger to persist.
Though there are early reports of white tigers in India, the first lineage of captive white tigers
originated in what was known at the time as Rewa, (which is now Madhya Pradesh), from a
single male known as Mohan who was captured in 1951 (Thorton et al. 1966). The first breeding
of Mohan to Belgum, a wild orange female, was unsuccessful in producing a white offspring.
Mohan was subsequently bred to his daughter, Radha, produced from the previous cross. This
resulted in four litters, all producing white offspring (Thorton et al. 1966). It can be inferred that
Rewa, an F1, was heterozygous for the white coat allele. Thus the Rewa-Mohan cross gave
offspring of the union a 50% chance of being homozygous for and therefore expressing the white
coat allele. The white coat polymorphism is an autosomal characteristic inherited in a
Mendelian-recessive fashion (Thorton et al. 1966). Although inbreeding was prevalent in early breeding of white tigers, it is not essential to produce a white tiger. Because the trait follows a
Mendelian inheritance pattern, the coat can be propagated given that both parents are carriers of
the allele.
Although the white coat polymorphism can be obtained without inbreeding, it can be challenging
to manage inbreeding levels while also selecting for the white phenotype. Because of this
breeders often resort to inbreeding to ensure that the trait is maintained. Mismanaged breeding
practices have reportedly led to an increase in health problems in some white tigers, such as
strabismus, facial deformities and neurological defects (Roychoudhury and Sankhala 1978).
However, it remains unclear to what extent these abnormalities are due to inbreeding. Some have
suggested that some of these health concerns may be linked to the white phenotype itself. For
example, strabismus, which is caused by retinal nerve fibers connecting at the opposite side of
the brain rather that the same side, is found in carnivores that are homozygous for an allele
within the albino series such as Siamese cats (Gulliery and Kaas 1973). Examination of a white
tiger’s lateral geniculate nucleus of the brain, (a region involved in processing visual information
gathered by the retina), revealed a defect of the A1 layer similar to, though less severe than that
of the Siamese (Gulliery and Kaas 1973). Therefore, determination of the degree of involvement
of the white phenotype versus inbreeding is essential in order to develop a scientifically based
breeding strategy for white tigers.

Though pigmentation and neurological development may seem unrelated, they are both derived
from the neural crest during the embryonic development of vertebrates (Rawles 1947).
Melanocyte precursors develop from the neural crest and spread to the hair and skin and 8
synthesize melanin (Rawles 1947). There are 2 forms of melanin: pheomelanin which produces
red or yellow pigment and eumelanin responsible for producing black or brown pigment
(Pawelek et al. 1982). These 2 types of melanin are structurally distinct; melanocytes producing
eumelanin tend to be more rounded than those producing eumelanin (Pawelek et al. 1982). White
tigers lack function in melanocytes producing pheomelanin, causing them to lack pigment where
other tigers would be orange. They carry pigment in their stripes which are gray or chocolate and
their eyes are blue. Therefore, white tigers are not albinos, though the coat of the white tiger is
due to an autosomal recessive mutation of the chinchilla allele, cch, and that locus is near the
albino locus (Robinson 1968).

The need for adequate levels of genetic diversity is a particular concern for endangered
populations, primarily due to magnified effects of genetic drift and deleterious alleles as
compared to larger populations (Hedrick and Kalinowski 2000). In a natural environment
species that suffers from severe inbreeding faces an increased likelihood for extinction.
However, in a captive environment these alleles are able to persist for much longer due to
protection from outside threats (Lacy 1987). Therefore, it is equally important to maintain high
genetic diversity in both captive and wild populations, not only for the salvation of a species, but
also for the health of individuals.
There is a well-established correlation between heterozygosity and traits determining fitness,
such as weight, fecundity and developmental stability (Milton and Grant 1984). Subsequently,
the overall health of a population can be inferred by examining the heterozygosity of the
population in question. Populations with lower heterozygosity are also at greater risk for disease
acquisition. A classic example of the effects of decreased genetic diversity is the cheetah,
Acinonyx jubatus . which occurred as a result of a historic bottleneck. This lack of genetic
diversity has led to difficulties in captive breeding due to abnormalities of the spermatozoa
(O’brien et al. 1985). Furthermore, the major histocompatibility complex, (MHC), is identical in
cheetahs making the population susceptible to pathogens (O’brien et al. 1985)

Based on the data gained from our microsatellite analysis, it is apparent that among the white tigers and orange tigers sampled, there is no statistically significant difference in heterozygosity. This indicates that the white tigers included in this study were likely outbred to orange tigers, maintaining higher heterozygosity. Though it is known that early captive white tiger populations originated through inbreeding, (Thorton et al. 1966), it is clear from our results that not all white tigers presently in captivity are significantly inbred. In an effort to broaden our understanding of genetic diversity among white tigers and orange tigers, we will continue to incorporate additional individuals and microsatellites, adding more power to our data.

CONCLUSION
Based on the analysis of 12 microsatellites, we have determined that there is not a significant difference between white tigers and orange tigers in terms of heterozygosity. As this study progresses, more microsatellites will be added in order to understand the levels of heterozygosity at other loci. More individuals will also be incorporated into this study to broaden our
understanding of the heterozygosity within captive-bred tigers. Evidence suggesting that white
tigers are not inbred to a significantly greater degree than orange tigers could potentially alleviate
some of the controversy surrounding the breeding of white tigers. More importantly, it will
provide breeder with data that is necessary in order to make critical management decisions that
affect both species and individual health.  A causal mutation has not been discovered in ASIP or MC1R, but their assessment has nonetheless been important in the search for the genetic origin of the white coat phenotype. We will continue our analysis by sequencing exon 3 of ASIP and TYR and possibly other candidate genes. Finding the gene responsible for this phenotype will provide new insight into the diversity and well-being of tigers. This information will be used to if there is a link between the phenotype itself and the health concerns sometimes appearing in white tigers.
As the tiger population continuously decreases in the wild, it becomes increasing apparent that we must ensure the welfare of the tigers in captivity. As a flagship species, the tiger serves as an ambassador for tigers in the wild, as well as conservation in general. Through increased research we can gain the knowledge necessary to protect the beloved white tiger and ensure that white tigers are carefully bred using the a management strategy that is genetically based.

For Access:  http://repository.tamu.edu/bitstream/handle/1969.1/148870/CARNEY-THESIS-2013.pdf?sequence=1

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