Codon bias in Ras-induced tumors: A Drosophila model
Public Deposited- Last Modified
- February 26, 2019
- Creator
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Paramore, Sarah
- Affiliation: College of Arts and Sciences, Department of Biology
- Abstract
- In humans, members of the RAS gene family are mutated in many cancers. There are three homologous RAS genes: HRAS, NRAS, and KRAS. These genes are greater than 90% identical in amino acid sequence. However, KRAS has a rare codon bias while HRAS and NRAS feature common codons. Interestingly, KRAS is mutated far more frequently in human cancers than either HRAS or NRAS. Therefore, identifying genes regulating codon biased mRNAs or proteins could provide insights into how KRAS functions as a potent oncogene. In order to identify these genes, I took part in a deficiency screen in Drosophila. By driving either rare or common RAS constructs in the eye, can identify deficiencies that differentially modify the eye tumor phenotype, eventually identifying specific genes. We have currently identified deficiencies that differentially modify the common and rare phenotypes, showing that our model works. Following up on our screen, I have identified Ribosomal Protein S21 as a key gene within a modifying deficiency as our first candidate regulator of RAS codon bias.
- Date of publication
- spring 2015
- Keyword
- DOI
- Resource type
- Rights statement
- In Copyright
- Note
- Funding: None
- Advisor
- Peifer, Mark
- Degree
- Bachelor of Science
- Honors level
- Honors
- Degree granting institution
- University of North Carolina at Chapel Hill
- Extent
- 23
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