Hardy-Weinberg Equilibrium: A Genetic Analysis

Population genetics is a useful biological tool that allows scientists to not only see genetic variation within a single population, but to also discover inconsistencies between the genetics of two different populations. Comparing the population genetics of two populations can reveal significant differences in their allele frequencies and thus expose meaningful biological variability between the two groups (1). Alleles, or the alternative forms of a gene, are direct indicators of variation within species and populations (1). The relationship between alleles and genotypes can be analyzed using the Hardy-Weinberg Equilibrium (1). The Hardy-Weinberg Equilibrium is a concept in which genetic variation remains constant within a population, if a

Gustatory cells on our tongues are full of taste receptors, coded for by all different genes, that bind to specific substances, and each of these three chemicals has a different receptor (1). These receptors bind to the PTC, Thiourea or Sodium Benzoate in order to activate neurons that signal to our brains that we can taste that particular chemical (1). The allele that codes for the tasting of each of these substances is dominant (T)(1). Our genes, which code for these taste receptors, were compared to the known North American genotype and allele frequencies for the same

TAS2R38 has 3 single nucleotide polymorphisms that are linked on the gene and inherited together as a haplotype (2). These three single nucleotide polymorphisms result in a change in DNA sequence, which means new amino acids and thus different protein folding (2). The three differences that exist from taster to non-taster are changes from a proline to an alanine, respectively, in one place on the sequence, an alanine to a valine within the binding pocket of PTC, and a valine to an isoleucine further downstream (2). The most significant change is the change of alanine (262) to valine. PTC, when in the pocket of the taste receptor, forms hydrogen bonds with alanine (262) and tyrosine (199) (2). When this occurs, PTC is bound tightly enough so that the neuron is activated, a signal is sent to the brain, and PTC is tasted (2). For non-tasters, the replacement of a valine results in a new conformation of the binding pocket (2). Consequently, PTC enters the pocket in a different orientation and forms only one hydrogen bond to a cysteine (2). This bond is not tight enough to activate the neuron and signal to the brain that PTC is