Presentation Type
Poster
Faculty Mentor’s Full Name
Ekaterina Voronina
Faculty Mentor’s Department
Biology
Abstract / Artist's Statement
Liver disease is becoming a more prevalent problem in the United States. Roughly 30 million Americans suffer from a form of it. The increase in obesity is causing non-alcohol related fatty liver disease in 20-30% of adults. Other causes can be viral infections such as Hepatitis A, B or C, immune system problems, genetic inheritance, cancer and over consumption of toxins. These issues, and more, contribute to scarring on the liver not allowing it to regenerate until it can no longer function. One way we can help fight this disease is by gaining a better understanding of its origins. This can be done by running tests in a lab on different proteins associated with the disease and recording their affects. For this we will be conducting tests on. elegans. These worms contain many orthologous proteins that share the same phenotype responses when disrupted as we would expect to see in humans. I will be using RNAi, to knock out 2 genes associated with liver disease in worms, mars-1 and dnj-29. The total number of genes associated with liver disease in OMIM was 3. This was the same number that was orthologous to humans. MARS-1 is in the cytosol and works with methionine and RNA ligase activity. This may affect the translation process in the cells. When this gene is knocked down, I would expect to see embryonic lethality. DNJ-29 is involved in protein translocation and is critical for cell function. Knocking this gene down should result in worm death. For either protein any change in the phenotypical response of the worm would be regarded as a victory. In dnj-29(RNA-i) this may take a generation to take place.
Category
Physical Sciences
C. Elegans and Liver Disease
UC South Ballroom
Liver disease is becoming a more prevalent problem in the United States. Roughly 30 million Americans suffer from a form of it. The increase in obesity is causing non-alcohol related fatty liver disease in 20-30% of adults. Other causes can be viral infections such as Hepatitis A, B or C, immune system problems, genetic inheritance, cancer and over consumption of toxins. These issues, and more, contribute to scarring on the liver not allowing it to regenerate until it can no longer function. One way we can help fight this disease is by gaining a better understanding of its origins. This can be done by running tests in a lab on different proteins associated with the disease and recording their affects. For this we will be conducting tests on. elegans. These worms contain many orthologous proteins that share the same phenotype responses when disrupted as we would expect to see in humans. I will be using RNAi, to knock out 2 genes associated with liver disease in worms, mars-1 and dnj-29. The total number of genes associated with liver disease in OMIM was 3. This was the same number that was orthologous to humans. MARS-1 is in the cytosol and works with methionine and RNA ligase activity. This may affect the translation process in the cells. When this gene is knocked down, I would expect to see embryonic lethality. DNJ-29 is involved in protein translocation and is critical for cell function. Knocking this gene down should result in worm death. For either protein any change in the phenotypical response of the worm would be regarded as a victory. In dnj-29(RNA-i) this may take a generation to take place.