Lethal alleles are those that fail to successfully code for the proper production of a functional protein that is vital for life. Recessive lethal alleles are mutations that are only lethal to homozygous individuals with two copies of the mutated allele (Castle, 1910) . In humans cystic fibrosis and sickle cell anemia are two examples of recessive lethal alleles. A dominant lethal allele is a mutation that is lethal to any individual that has one or two copies of the allele. Huntington disease is an example of a dominant lethal allele, it is maintained in the population because of the late onset of death.
Sub lethal alleles are those that cause death in only some carriers of the gene, an example of this is hemophilia here the male who has an affected X chromosome, will only die if he is affected by trauma to the body, otherwise he will stay healthy. Zee Mays has a lethal recessive allele for albinism; which in homozygous causes a plant to grow with zero chlorophyll and to undergo death very fast. Heterozygous are the carriers for this trait since the recessive homozygous are killed. The heterozygous for the “L” allele are green since they produce chlorophyll.
The aim of the Zee Mays investigation was to distinguish lethal alleles by reviewing observing frequencies in growth. In order to do this, dominant and recessive alleles had o be observed. In Zee Mays deleterious alleles cause a loss of function through the deletion of a vital part of the gene that codes for chlorophyll. Deleterious alleles have a normal phenotype in heterozygous. Deleterious alleles can have a disease fighting effect where it is more beneficial for an individual to have the heterozygous form; this is the case in sickle cell disease and cystic fibrosis.
In sickle cell disease the heterozygous individual is protected against malaria, and an individual with the CUFF trait is protected from Typhoid. This is known as heterozygous advantage (Uncle, 2004). Slightly deleterious alleles remain in the population for much longer than purely deleterious alleles; these alleles are maintained through drift and in small populations (Sundaes, 2000) . Thus the frequency of deleterious alleles falls drastically with each generation, compared to the slightly deleterious allele.
Background The purpose of this experiment was to observe the phenotypes frequencies of the Zee Mays, in order to do that we had to plant and observe generations of the species. We were looking for a ratio of albino plants that died very quickly after growth, to decrease proportionally. The expected proportions were 3: 1 Rene: albino for IF; 35:1 for IF; and 64:1 for IF. The process for planting was that outlined in the lab manual with the following changes. We planted 32 IF, 5-6, and IF plants in week 2. We used a 50:50 mix of vermiculite and peat elite. We first filled the units 3/4 full with soil then added IL water. Ext we planted our seeds, 4 per cell. Next we added the soil to cover to the top of the cells. Finally another 1. 5 L of water was added to the trays via the bottoms. Cell UNIT Fig. 1 This figure illustrates the planting scheme used. Predictions and Hypotheses Before the counts were performed it was predicted that the Albino allele q or endnote PI would decreasingly become less pronounced in the population. It was also predicted that the population would maintain its numbers of the heterozygous or green corn plants that possessed the p allele or Pl genotype.
The null hypothesis was that the albino plants would maintain allele frequencies consistent to those at Hardy-Weinberg Equilibrium. The hypothesis being tested was whether the allele frequencies of a double heterozygous cross between two Law/Law individuals changed over time, focusing on the q or albino allele; determine whether it was conforming to the Hardy-Weinberg Equilibrium Model ND not steadily declining in the population as a lethal allele. Predictions and Hypotheses After IF After harvesting. IF generation it was many predictions were viable.
The first prediction is that the albino allele will continue in the population at a decreasing rate due to maintenance by those who germinate with it before its death. It is also predicted that the albino allele will become fixated near or at zero. Discussion and Conclusion Overall the data are inconclusive, Figure 2 illustrates the expected frequency distribution overtime and how the albino allele will become fixated within the population. The fixation of this allele approaches zero. Tables 1-3 illustrates the scoring of the class data for the Zee Mays.
Table 4 is the calculations used in finding the chi square goodness of fit test to determine whether the albino allele was conforming to the Hardy-Weinberg Equilibrium Model and not steadily declining in the population as a lethal allele. Because our Chi square calculated > Chi square critical value, there is a statistical difference between the observed number so individuals and expected number of individuals surviving with the albino allele, under HOW equilibrium conditions, That is you reject the lull hypothesis and conclude the population is not under HOW equilibrium in the Law/law locus of the Zee Mays population.
Table 6 summarizes these results. TWO main future directions for this experiment include expanding the experiment into further generations and using different varieties of maize to utilize the aspects of hybrid vigor ( (Saleroom, 2007). Expanding the experiment further will allow the scientist to see whether the allele is fixated or lost all together. Using multiple subspecies of maize will allow the scientist to learn if there is predominance or single locus heterodox going on as well as many other heartsickness at the population level (Saleroom, 2007).