Two problems plagued linear chromosomes: loss of terminal DNA sequence with each cell cycle and chromosome end fusions. Telomeres protect the genome from these lethal effects. However, while the proteins that make up the telomere are rapidly evolving, the function of the telomere to protect remains unchanged. This paradox establishes the basis of my research this summer under the mentorship of Dr. Mia Levine and her lab. Of the many proteins discovered that follow this paradox, the nucleosome assembly protein-1 (nap-1), necessary for keeping chromosomes separated rather than fused, became my gene of interest. Using the closely related Drosophila melanogaster (D.mel) and Drosophila simulans (D.sim) flies, I studied the functions of the nap-1 gene. Three amino acids – components of proteins - were changed using CRISPR technology in the mutated nap-1 allele, which was then inserted into D.sim. To study the paradox and understand the significance of these three quickly changing amino acids, I used the Position Effect Variegation and Telomeric Position Effect techniques by crossing flies carrying a white gene - which expresses the phenotype for red eyes – with heterozygous D.mel and D.sim flies. Then, I imaged and measured the amount of red pigmentation on the eyes of the male children. My data suggests that the mutated allele does cause a disruption at the end of the chromosome. A test for viability was then set up to test the biological costs of such a disruption; the amino acid changes in the D.sim allele observe that all its homozygous genotype flies are dead.
But besides being able to put the above content of my project on a poster to present to others, this experience has been meaningful for my academic experience. I learned other techniques relevant to fly work and molecular biology. I learned to dissect larval salivary glands and brains, and testes. With my lab manager, we helped treat infected flies with antibiotics. I was shown how the cloning process works. Aside from the practical skills, I have learned to enjoy biology for itself, because the process of scientific discovery is exciting. And this experience has helped influence my choice of major. Coming onto campus without prior research experience and being surrounded by a heavy pre-professional culture, I was not sure if I would ever have a chance to do research, a part of my academic experience that I have been looking forward to pursuing since high school. PURM made what I almost thought was possible only in thought but not in practice, possible.
Two problems plagued linear chromosomes: loss of terminal DNA sequence with each cell cycle and chromosome end fusions. Telomeres protect the genome from these lethal effects. However, while the proteins that make up the telomere are rapidly evolving, the function of the telomere to protect remains unchanged. This paradox establishes the basis of my research this summer under the mentorship of Dr. Mia Levine and her lab. Of the many proteins discovered that follow this paradox, the nucleosome assembly protein-1 (nap-1), necessary for keeping chromosomes separated rather than fused, became my gene of interest. Using the closely related Drosophila melanogaster (D.mel) and Drosophila simulans (D.sim) flies, I studied the functions of the nap-1 gene. Three amino acids – components of proteins - were changed using CRISPR technology in the mutated nap-1 allele, which was then inserted into D.sim. To study the paradox and understand the significance of these three quickly changing amino acids, I used the Position Effect Variegation and Telomeric Position Effect techniques by crossing flies carrying a white gene - which expresses the phenotype for red eyes – with heterozygous D.mel and D.sim flies. Then, I imaged and measured the amount of red pigmentation on the eyes of the male children. My data suggests that the mutated allele does cause a disruption at the end of the chromosome. A test for viability was then set up to test the biological costs of such a disruption; the amino acid changes in the D.sim allele observe that all its homozygous genotype flies are dead.
But besides being able to put the above content of my project on a poster to present to others, this experience has been meaningful for my academic experience. I learned other techniques relevant to fly work and molecular biology. I learned to dissect larval salivary glands and brains, and testes. With my lab manager, we helped treat infected flies with antibiotics. I was shown how the cloning process works. Aside from the practical skills, I have learned to enjoy biology for itself, because the process of scientific discovery is exciting. And this experience has helped influence my choice of major. Coming onto campus without prior research experience and being surrounded by a heavy pre-professional culture, I was not sure if I would ever have a chance to do research, a part of my academic experience that I have been looking forward to pursuing since high school. PURM made what I almost thought was possible only in thought but not in practice, possible.