Currently the Amon lab consists of a bunch of really awesome people!
Aneuploidy, defined as an unbalanced cellular karyotype, is associated with developmental defects and disease in all organisms studied to date. Models of aneuploidy in various systems indicate that an unbalanced karyotype leads to slowed proliferation and other phenotypic hallmarks of stress. However, aneuploidy is also strongly associated with cancer, a disease characterized by uncontrolled cell proliferation. Using our yeast model, consisting of haploid strains of S. cerevisiae that contain single extra chromosomes, I am working to characterize the molecular stresses caused by aneuploidy more completely in order to shed light on this paradox. I am using synthetic genetic array analysis to identify genes and pathways necessary for, or antagonistic toward, the growth of aneuploid cells in an unbiased and genome-wide manner, and investigating the role of these pathways in the biology of aneuploid cells.
Copy number variation (CNV) refers to increases or decreases in DNA content which can extend from single genes to whole chromosomes. Changes in DNA copy number lead to changes in gene expression and thereby alter cell physiology. While CNVs are widely documented in cancer cells, where they presumably mediate cellular transformation, the prevalence of CNVs in normal tissues, and their implications for tissue function, are poorly understood. I am using a combination of single cell sequencing, mouse models, and human samples to characterize CNVs in normal tissues, determine how they arise, and investigate their roles in organ physiology and disease.
Meiotic cell division is a hallmark of sexually reproducing species and Clb-CDK is a key regulator of this critical process. My research is aimed at elucidating the mechanisms by which the cell regulates translation in order to execute meiosis. In budding yeast, the Clb cyclins associated with the CDK Cdc28 govern progression through the meiotic cycle.