Introduction
The fruit fly, Drosophila melanogaster, became an important model organism for the study of human genetics and for the establishment of more biological principles (Roberts 2006). This organism became a good candidate to work with because of its short life cycle, its inexpensiveness, small size, its genetic variability, easily cultured and its ability to produce many offspring. Nichols and Phandey made an important discovery: approximately 75% of disease-causing genes in humans are homologous to genes found in Drosophila melanogaster (Russell and Tickoo). This is an important observation, because it made it possible to discover treatments for human diseases. For example, the fly has a tumor gene homologous to the human LATS1 gene.
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Both males and females are affected with this gene, making it autosomal. This mutation results in a light brown-pigmented eye instead of the red wild type eye. This is due to the lack of pigments in the eye that would normally give rise to the wild type eye color (Lloyd 1998). The eye color darkens when the fly starts to age. Although, this mutation primarily affects the eye color, it also changes other parts of the body. For example, the malphigian tubules are a pale yellow. The fly’s testes and vasa become colorless during their adulthood. A possible chromosomal effect on phenotype occurs when alleles are recessive. When these homozygous recessive alleles are present in a fly, they are …show more content…
The mutagen of this allele is spontaneous and results in a yellow-brown eye, which varies, from the regular brown eye in the mutation. After a couple days the eye darkens into a garnet color. Testes remain colorless, and the malphigian tubules are pale yellow. Smaller pigment granules are observed in the mutant. This allele is dominant and in chromosome 2. Additionally, the nature of the lesion is caused by the insertion of the 412-transposable element in the molecular structure of the gene in DNA. Besides affecting the eye color, it also creates a decreased sensitivity to chemical’s toxic effects in comparison to the wild type. These toxic effects include inebriation, sedation, sustained damage, developmental defects and death (Campbell and Nash,
The conducted experiment assists in determining an unknown mutant allele found in Drosophila melanogatser. Mutant 489 illustrates a defect in eye pigmentation, which displays a dark brown eye color verses the brick red eyes in wild type flies. Based on the appearance our 489 mutation we've names our mutant rust.
Introduction: The intention of this lab was to gain a better understanding of Mendelian genetics and inheritance patterns of the drosophila fruit fly. This was tasked through inspecting phenotypes present in the dihybrid crosses performed on the flies. An experimental virtual fly lab assignment was also used to analyze the inheritance patterns. Specifically, the purpose of our drosophila crosses is to establish which phenotypes are dominant/recessive, if the traits are inherited through autosome or sex chromosomes and whether independent assortment or linkage is responsible for the expressed traits.
4. Clear wing, Black eye, and Hairless (c, b, and h) are linked, recessive traits carried on
The materials and methods are adapted from Evolution Lab Manual, Lab One: The Fly Lab (Welsh, 2016). The stock bottles contained true breeding homozygous flies of either ebony body or wild-type body (tan). The fruit fly was observed because it is easily cultured, it has a two week generation time at 21-23°C, it occupies little storage space, and it is large enough to see phenotypic traits. Two cultures were set up with an equal number of flies with each trait, to start with an initial allele frequency of p=0.5.
When examining the D. Melanogaster mutants in the lab, our group immediately noticed an apparent difference from the wild-type flies. None of the mutants were able to fly. This led us to believe that we were dealing with a wing mutation. Upon further examination, we concluded that it was the overall wing shape that prevented the mutants from flying. The wing shapes among the mutants varied in both size and shape. Some were long, while others were short. The mutant wings could be distinguished into two general classes. One division of the mutant wing was short and stubby, almost a fourth the size of the wild-type wing. The rest of the mutants ranged in wing size and length, however many mutant wings were the same length as the wild-type wings. Although the
Purpose The purpose of this experiment is to determine whether the fruit flies were dominant/recessive or linked/non-linked. The traits I chose for this activity was the fruit fly with vestigial wings and purple eyes, the other fruit fly I chose was a normal fly, also called wild type. While writing out my plan for this activity I thought it would be interesting to test a female mutant and the wild type male, the ratios I came up for this experiment was 2:2 and the mutant allele being recessive to the wild type. In this case, the words recessive and dominant means, if the child born from the parents inherits more of the genes and traits from let us say the father then the alleles of the father is dominant over the mother’s genes.
The Drosophila melanogaster is a fruit fly with a very short life cycle. They can be winged or wingless, and have red eyes or white eyes. The different options are called alleles. Alleles are the variants of a specific gene, and one is received from each parent on each chromosome. (“What Are Dominant and Recessive?”). It was chosen to use winged females and wingless males to predict the offspring in this experiment. The winged allele is dominant, meaning it only needs one allele to physically appear. The wingless allele is recessive, which gets covered up by the dominant allele (“Fruit Fly Genetics”). Each trait has two alleles in the flies’
Fruit flies with normal wings have a higher population and greatly outnumber the population of fruit flies with dichaete or vestigial wings.
There were some sources of error in crossing between certain traits, specifically in determining the genotypes of the organisms being crossed. For example, there was no method of determining whether the wild type flies were homozygous dominant or heterozygous. The method used seemed reliable, but due to the questionable results, it may be more effective to find another
We will use Punnett Squares to find out the genotype and phenotype in the offspring of the fruit flies. Our experimental hypothesis of this experiment is that the genes of the fruit flies are linked, where the body color of the fruit fly is dark (b) recessive or light (B) dominant and type of wing, normal wings (W) dominant and abnormal wings (w) recessive is linked. The null hypothesis is that there will be an unlinked ratio for the phenotypes if the loci was
Fruit Fly experiment was conducted by using different techniques. One of the main things was to examine the fruit flies and identify the difference between females and males, identify their mutation if they were wild type, white eye, vestigial or white and vestigial combined together. These Fruit flies were kept in the incubator at 25°C for about 6 days. The main goal for this experiment was to observe the principles of Mendelian genetics.
In this experiment we tested to see what the offspring of an unknown cross of an F1 generation would produce. After observing the F2 generation and recording the data we found some of the Drosophila showed mutations, two in particular. The mutations were the apterus wings, and sepia eyes. After collecting our data through observation, a Chi-test was conducted resulting in a Chi-value of 5.1 and a p-value of .2. Since the p-value was greater than 0.05, there was no significant change in the data. This proved that the Drosophila flies still followed the Mendelian genetics of a 9:3:3:1 ratio.
Throughout this experiment a number of random and procedural errors were apparent; these errors could have affected the results of the experiment in a number of ways. One experimental error that occurred during the experiment was that some flies became stuck in the food source and died. The main cause of this was the fact that the fly vials were stood up (vertically) before the flies had fully recovered from the anaesthetic. This could be overcome in future experiments by ensuring that the vials are kept horizontal until all of the flies fully recover from the anaesthetic.
Based upon observation of the F1 generation, we hypothesize that the inheritance of the white-eye (W) mutation is sex-linked and recessive wild type.
Three other genes make proteins that are also involved in melanin pigment formation and albinism, but the exact role of these proteins remains unknown. These genes are the P gene on chromosome 15, the Hermansky--Pudlak syndrome gene on chromosome 10, and the ocular albinism gene on the X chromosome.