| dc.description.abstract | The white phenotype in tigers is highly sought after by zoos and private sanctuaries. There are enough animals in the captive population to avoid severe inbreeding, however close relatives are often bred together to produce the elusive white phenotype. Heritable disorders in white tigers have been noted, for example strabismus, cleft palate, and spinal and facial defects. These are linked to the white phenotype and likely caused by inbreeding. It is important to determine the genetic basis of the white coat color and associated disorders so that breeding could be modified to avoid these detrimental phenotypes.
We used information obtained from other species regarding the genes found to be involved to select two likely candidates for the white phenotype in tigers, MC1R and ASIP. Both melanocortin-1-receptor (MC1R) and Agouti Signaling Protein (ASIP) affect the relative amounts of pigments produced by the melanocytes. MC1R controls the peptide hormones melanocortins that determine the type of melanin produced by the melanocyte. ASIP is the antagonist for MC1R, deactivating alpha-melanoctye stimulating hormone, which leads to increased phaeomelanin production, while loss of activity of ASIP results in eumelanin.
We isolated DNA from four white, one snow white, and fourteen orange tigers. We then Sanger sequenced ASIP exon 1 and 2 for these various tigers as well as several other felid species. We then compared the ASIP sequences is felids to several families of primates. Sequences were aligned in MEGA and the nucleotide and amino acid differences were compared. This analysis showed no difference between the various tiger coat colors in ASIP. This leads us to believe that ASIP is not responsible for the white coat color in tigers. | en |
