Ribosomes, Cell Competition, and Cancer

The Baker lab will be moving to UC Irvine in 2024. A PhD position is available to elucidate molecular mechanisms of ribosomopathy, cell competition, and cancer. We are specifically interested in the properties and behavior of cells that lose copies of ribosomal protein genes. This happens in the disease Diamond Blackfan Anemia, and in the early stages of aneuploidy and cancer, where Rp gene mutations occur in 43% of human tumors. Aneuploid cells, which may lose whole chromosomes that include ribosomal protein genes, are found in most cancers. During development, cell competition recognizes and eliminates these abnormal cells and is thought to regulate aging and cancer development. Our research will address the role of cell competition in preventing accumulation of aneuploid cells in aging and the development of cancer, the genes that are required for cell competition, the mechanism whereby abnormal cells are recognized by their neighbors, and the molecular mechanisms of disrupted ribosome biogenesis in cancer. The student will employ genetic, molecular genetic, and biochemical approaches, including ribosome profiling, single cell sequence analyses of gene expression, whole genome analysis of aneuploidy and of mutation accumulation, and lineage analysis in transgenic Drosophila, mouse, and human cell models. Applicants should be committed to contributing to demanding and cutting edge research and have or soon expect to receive a PhD or equivalent with relevant experience. Please attach a CV along with contact information for three academic references along with your application. Apply early for fullest consideration.
References
Baker, N.E. (2020) Emerging mechanisms of cell competition. Nature Reviews Genetics 21; 683-697.
Baker, N.E., and Montagna, C. (2022). Reducing the aneuploid cell burden: cell competition and the ribosome connection. Dis Models Mech 15:dmm049673.
Kiparaki, M. and Baker, N.E. (2023) Ribosomal protein mutations and cell competition: Autonomous and non-autonomous effects on a stress response. Genetics, 224:iyad080.